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How can I reduce my IgE level?

Abstract – IgE secretion by B lymphocytes defines the allergic state and nearly all asthmatics have higher than normal IgE levels in serum following adjustment for age and sex. It is thought that allergic mechanisms may be responsible for the increasing prevalence of asthma.

In particular, in utero changes may encourage T cells to differentiate into Th2 subtypes. Th2 cells produce cytokines such as IL-4 and IL-5, which can act indirectly via B cells, mast cells and eosinophils to mediate the asthma phenotype. Alternatively, IL-4 and IL-13 may act directly on the airway. Th2 lymphocyte inflammation in asthma predisposes subjects to B cell and IgE-mediated airway inflammation.

IgE binds to receptors on the surface of a variety of effector cells causing them to release a variety of mediators that promote airway hyperresponsiveness, mucus secretion and increased vascular permeability. Several strategies for decreasing IgE have been developed as a possible treatment for asthma.

For example, anti-IgE monoclonal antibodies such as rhuMAb-E25 and CGP 56901 block binding of IgE to its high-affinity receptor and have been shown to reduce IgE levels in humans without causing anaphylaxis. IgE levels must be nearly completely suppressed. Recent clinical studies in subjects with asthma have shown that rhuMAb-E25 attenuates both the early and late phase responses to inhaled allergen, and reduces the associated increase in eosinophils in induced sputum.

rhuMAb-E25 is well tolerated and has shown promising results in improving symptoms and lung function in patients with moderate to severe asthma. Other strategies for decreasing IgE levels include interferon gamma, IL-4 antibodies, IL-4 receptor antibodies and soluble IL-4 receptors.

What foods reduce IgE levels?

Summer ushers in blue skies, blooming flowers and trees, birds chirping and bright green grass. But for some of us there are other things that come along with the change in seasons – itchy eyes, runny noses, sneezes galore, stuffy heads, and clogged sinuses that make you feel miserable.

• Ah, seasonal allergies.
• With all the blooming and flowering going on, our immune systems kick into overdrive as the pollen count begins to skyrocket.
• For many of us, that means we rely on a cocktail of antihistamines, eye drops, and tissues until we can breathe freely again.
• But don’t hit the medicine cabinet just yet.

Your summertime allergy relief might be as close as your kitchen. Many fruits, vegetables, spices, and herbs are natural allergy fighters, thanks to the potent antioxidants, vitamins, minerals, and anti-inflammatory properties found in these foods, they help bolster your immune system and reduce the impact of allergies.

• In fact, food has been used as medicine for many, many years and in traditional cultures before synthetic drugs were available.
• And when you use food as medicine, you can help your body return to a state of optimal health.
• Here are five allergy-fighting foods that may help to ease your seasonal allergies: 1.

Kale This leafy green vegetable has been in the spotlight over the past few years, and for good reason. Kale is a good source of magnesium, an essential mineral that affects how hundreds of different enzymes act in your body and may protect against inflammation. Check out our Kale+ shot which is perfect for reviving and restoring your body.2. Strawberries Strawberries are a rich source of fisetin, an anti-inflammatory and antioxidant flavonoid that keeps your immune system functioning properly. Scientists in Korea found that fisetin inhibited histamine release and the expression of pro-inflammatory markers in the body. Check out our Strawberry Shines juice, which has all of those important vitamins and nutrients to help support a healthy immune system, it’s also great for your skin! 3. Turmeric The brightly colored spice, common in South Asian cooking, has been used in Ayurvedic practices for centuries. Check out our Turmeric Super Shots, which are great for those important anti-inflammatory and antioxidant properties.4. Broccoli Broccoli might resemble the trees that may be the root cause of your seasonal allergies, but the green veggie also contains powerful anti-allergy properties.

1. In fact, researchers have found that a compound in broccoli increased the presence of the enzyme glutathione-S-transferase, a vital antioxidant that helps detoxify the body and may reduce inflammation.
2. In a separate study, other scientists have found that the broccoli compound may also blunt the allergy and asthma-inducing impact of diesel exhaust.5.

Green tea Green tea has been touted for its health and immune-boosting benefits for years. That’s because tea is rich is catechins, a natural compound in the flavonoid family. Researchers from the University of California, Davis, showed that the active ingredient in green tea enhances the function of regulatory T-cells, which help keep your body’s inflammatory response in check.

Other studies have found that green tea lowers blood levels of the IgE antibody, a compound that’s a prime player in the body’s allergic and inflammatory response. Food plays an important role in helping our bodies bolster its natural defences. And, as these examples highlight, these powerful allergy fighters can easily be incorporated into your daily meals.

Stay Safe, The B.Fresh team

Can vitamin D deficiency cause high IgE?

Discussion – In this study, both groups had deficient levels of vitamin D. The study group with allergic rhinitis had significantly lower mean levels of serum vitamin D as compared to the control group. However, upon stratification, the results were weakly insignificant. IgE, which mediates allergic immune responses, has been shown to have an inverse relationship with serum vitamin D levels. Patients with low levels of vitamin D have high levels of IgE, IgE is the basis of all allergic responses. There have been various reports of AR in children and adults with low levels of vitamin D, Similarly, there have been reports of antenatal maternal vitamin D deficiency with a higher incidence of atopy in newborns, The Nord-Trøndelag Health Study (HUNT) was a longitudinal cohort conducted in Norway. It collected serum vitamin D levels at baseline and then followed the individuals for around 11 years. In men, 9% developed AR; the adjusted odds ratio (AOR) was 2.55 at vitamin D <50nmol/L. In women, 15% developed AR; however, the AOR was 0.83 for each 25 nmol/L reduction in vitamin D levels, Hence, another hypothesis came forward that there might be different impacts of vitamin D on AR development in men and women. As with our study, there have been other studies in the literature, which showed little to no impact of vitamin D deficiency on the development or worsening or AR. In a study with Turkish children, mean vitamin D levels in the AR group were 18.07 ± 6.1 ng/mL, as compared to 14.81 ± 4.86 ng/mL in the non-allergic rhinitis (NAR) group, and 24.03 ± 9.43 ng/mL in control group (p=0.001). More children in NAR were vitamin D deficient as compared to AR 67% vs.89%). Vitamin D levels did not statistically correlate to allergen sensitivity and AR duration and severity, Similarly, in a Korean study group, mean serum vitamin D levels were significantly lower in patients with atopic dermatitis but not asthma, AR, or IgE sensitization, Some interventional studies have highlighted the role of supplementation of vitamin D in the alleviation of AR symptoms. In Heine et al., vitamin D supplementation in vitamin D deficient mice resulted in immunomodulation, which favored protection against allergic triggers. Production of pro-inflammatory cytokines was reduced and that of anti-inflammatory cytokines was increased by vitamin D supplementation, Jerzynska et al. supplemented children with vitamin D during the pollen season and observed fewer manifestations of AR as compared to the placebo group, The study has its limitations. Firstly, the sample size was small. A large proportion of the study sample was outdoors. which was thought to bring a bias on higher vitamin D levels to the study (due to sun exposure); however, most participants in both study groups had lower vitamin D levels. We recommend further studies with the control group selected on the basis of blood analysis and eliminating individuals with low vitamin D levels. This will bring more strength to the study mythology, however, it was not possible in our case due to limited resources.

What is the root cause of high IgE?

Elevated serum immunoglobulin E(IgE) can be caused by allergies, infections and immune conditions including hyper IgE syndrome (HIES).

Does Omega 3 reduce IgE levels?

Omega-3 fatty acids decrease IgE-mediated activation of mast cells in several animal models and in human cells.

Does ginger reduce IgE level?

Ginger extracts decreased the level of total serum IgE We observed a boosted level of total IgE level in sera of mice exposed to ovalbumin (p

Can exercise lower IgE levels?

It has also been suggested that moderate-intensity physical training may induce a decrease in both total and allergen-specific IgE levels.

Can turmeric reduce IgE level?

Turmeric (Curcuma longa) attenuates food allergy symptoms by regulating type 1/type 2 helper T cells (Th1/Th2) balance in a mouse model of food allergy , 4 December 2015, Pages 21-29 Turmeric ( ) has traditionally been used to treat pain, fever, allergic and such as,, and dermatitis. In particular, turmeric and its active component,, were effective in ameliorating immune disorders including allergies.

However, the effects of turmeric and curcumin have not yet been tested on, Mice were immunized with intraperitoneal (OVA) and alum. The mice were orally challenged with 50 mg OVA, and treated with turmeric extract (100 mg/kg), curcumin (3 mg/kg or 30 mg/kg) for 16 days. Food allergy symptoms including decreased rectal temperature, diarrhea, and were evaluated.

In addition, cytokines, immunoglobulins, and mouse mast cell protease-1 (mMCP-1) were evaluated using, Turmeric significantly attenuated food allergy symptoms (decreased rectal temperature and anaphylactic response) induced by OVA, but curcumin showed weak improvement.

• Turmeric also inhibited IgE,, and mMCP-1 levels increased by OVA.
• Turmeric reduced type 2 helper cell (Th2)-related cytokines and enhanced a Th1-related cytokine.
• Turmeric ameliorated OVA-induced food allergy by maintaining Th1/Th2 balance.
• Furthermore, turmeric was confirmed anti-allergic effect through promoting Th1 responses on Th2-dominant immune responses in immunized mice.

Turmeric significantly ameliorated food allergic symptoms in a mouse model of food allergy. The turmeric as an anti-allergic agent showed immune regulatory effects through maintaining Th1/Th2 immune balance, whereas curcumin appeared immune suppressive effects.

• Therefore, we suggest that administration of turmeric including various components may be useful to ameliorate Th2-mediated allergic disorders such as food allergy, atopic dermatitis, and asthma.
• Allergic reactions occur when the immune system overreacts to normally harmless substances in the environment.

This hypersensitivity occurs in various forms including atopic dermatitis, asthma, allergic rhinitis, and food allergies. The incidence of allergic reactions has been increasing every year. In particular, food allergies have been estimated to affect ~6% of children and ~4% of the adult population (Sampson, 1976, Venter et al., 2008).

To treat or prevent allergic disorders, many studies are currently in progress, and many drugs have been developed such as immunosuppressants, antihistamines, and steroids (Wong et al., 2013; Kim et al., 2013; Conen et al., 2013). Although these drugs are effective, when taken for long periods, these drugs may have adverse effects such as growth retardation, diabetes, hypertension, cataracts, and osteoporosis (de Benedictis and Bush, 2012; Elphick and Southern, 2012).

Due to these potential problems, natural products may provide an alternative to effectively treat allergies with fewer adverse effects. The rhizome of Curcuma longa Linn., called turmeric (given the name curry spice by the British), has been widely consumed as a seasoning and used for the treatment of inflammatory disorders in gastrointestinal and respiratory systems in Asian countries such as China, Japan, Korea, and India (Srinivasan, 1953; Gilani et al., 2005).

1. Turmeric has been also studied expansively for its pharmacological activities such as antioxidant, anti-inflammatory, anti-cancer, anti-microbial, and neuroprotective effects (Toda et al., 1985; Chandra and Gupta, 1972; Kuttan et al., 1985; Lutomski et al., 1974; Rajakrishnan et al., 1999).
2. Curcumin, a main ingredient derived from turmeric, has been also claimed to be an antioxidant and anti-inflammatory agent (Balasubramanyam et al., 2003; Aggarwal et al., 2007).

The immunoregulatory activities of curcumin have been extensively studied since they were first reported in 1999 (Antony et al., 1999). For example, curcumin attenuated allergic airway inflammation by regulating the balance of CD4 + CD25 + regulatory T cells (Tregs) /T-helper (Th) in ovalbumin (OVA) -sensitized mice (Ma et al., 2013).

In allergic disorders, turmeric and curcumin ameliorated allergic rhinitis (Thakare et al., 2013), asthma (Oh et al., 2011), food allergy (Mathias et al., 2013), allergic conjunctivitis (Chung et al., 2012), and allergic contact dermatitis (Thompson and Tan, 2006) through regulation of Th2-, immunoglobulin E (IgE) – and mast cell-mediated immune responses.

However, especially in food allergy, it has not been known whether turmeric and curcumin can attenuate allergic responses to food in a mouse model of food allergy, and also how they regulate. Therefore, we investigated the effects of turmeric and curcumin as a positive control on T cell-mediated immune responses in an OVA-induced mouse model of food allergy.

RPMI 1640 medium, fetal bovine serum, penicillin-streptomycin, and Dulbecco’s phosphate-buffered saline (D-PBS) were purchased from WelGENE (Daegu, Korea). OVA (grade VI), red blood cell lysis buffer, and curcumin were purchased from Sigma-Aldrich (St. Louis, MO, USA). Turmeric used in this study was purchased from Kyeong-dong Oriental Pharmacy (Seoul, Korea) and identified by Professor Y.

Bu, Department of Herbal Pharmacology, Kyung Hee University. The specimen (KFRI-SL-1005) has been stored at Turmeric extract is traditionally used for the treatment of pain, fever, allergic and inflammatory diseases such as bronchitis, arthritis, and dermatitis.

• However, the scientific proof for anti-allergic effects of turmeric extract is not clear, especially for food allergy.
• In this study, we examined the anti-allergenic effects of turmeric extract with curcumin as a positive control in a mouse model of food allergy.
• Th2 cells producing IL-4, IL-5, and IL-13 play a critical role in the initiation In this study, we investigated anti-allergic effects of turmeric extract and curcumin in a mouse model of food allergy (Fig.1).

We treated mice with 100 mg/kg body weight of turmeric extract by oral gavage because of biological activity of turmeric extract (Ishita et al., 2004). And 3 mg/kg body weight of curcumin administered by oral gavage to mice because turmeric extract contains about 3% curcumin (Tayyem et al., 2006).

Therefore, the turmeric extract and curcumin L groups provided the same In the present study, turmeric extract significantly attenuated OVA-induced food allergic symptoms, whereas curcumin, an active component of turmeric, showed a tendency to reduce allergic symptoms in a mouse model of food allergy.

Turmeric extract regulated immune responses to maintain Th1/Th2 immune balance, although curcumin treatments showed immune suppressive effects. Therefore, the turmeric extract, which includes various active components as well as curcumin, can be used as an The authors have no conflict of interest to declare.

S. Bischoff et al. A.H. Gilani et al. M. Karaman et al. R. Kuttan et al. H. Lee et al. J.H. Lee et al. C. Ma et al. D.O. Moon et al. O. Naksuriya et al. S.W. Oh et al.

K. Reyes-Gordillo et al. S. Sharma et al. S.H. Sicherer et al. Subhashini et al. V.N. Thakare et al. R. Wong et al. B.B. Aggarwal et al. R. Aldini et al. S. Antony et al. M. Balasubramanyam et al. D. Chandra et al. S.H. Chung et al. S. Conen et al. F.M. de Benedictis et al.

This study aimed to explore the underlying mechanism about combined thermal/pressure processing on the allergenicity of shrimp ( Macrobrachium nipponense ). We analysed sensitizing and eliciting capacities, structural changes, gastrointestinal digestion, and mapped linear epitopes. Mice treated with steamed + reverse-pressure sterilized shrimp exhibited lower specific IgE and IgG 1 concentrations, degranulation, vascular permeability, and allergic symptoms than those fed with raw shrimp or steamed shrimp ( p < 0.05). Reduced allergenicity of shrimp using combined thermal/pressure processing was not only associated with protein unfolding and exposure of hydrophobic residues, but also related to disruption of immunodominant linear epitopes (Glu177-Ser188 in tropomyosin, Gln361-Ser366 in β-actin) due to changes in gastrointestinal digestion behavior. Moreover, heat/digested stable epitopes of arginine kinase were located inside its 3D structure, preventing binding with IgE and maintaining hypoallergenicity following combined processing. Thus, steaming and reverse-pressure sterilization might be an efficient low-allergenic food processing method for Macrobrachium nipponense, Premenstrual syndrome (PMS) and primary dysmenorrhea (PD) are common gynecological complications and there is evidence that inflammation may be an important factor in their etiology. There is a relationship between PMS and PD with susceptibility to allergic disorders. We aimed to assess the effect of curcumin co-administered with piperine on serum IL-10, IL-12 and IgE levels in patients with PD and PMS. A sample of 80 patients were recruited to this triple-blind, placebo-controlled clinical trial. Participants were randomly allocated to curcumin (n = 40) and control groups (n = 40). Each participant received one capsule (500 mg of curcuminoid plus piperine, or placebo) daily, from 7 days before until 3 days after menstruation for three consecutive menstrual cycles. Serum IgE, IL-10 and IL-12 levels were quantified by using an ELISA kit. No significant differences were found between the two groups at baseline, including: age, BMI, and dietary intakes ( P > 0.05). Curcumin + piperine treatment was associated with a significant reduction in the mean serum levels of IgE ; but there were no significant changes in the placebo group ( P = 0.12). Serum concentrations of IL-10 and IL-12 before and after the trial period did not differ significantly between the two groups ( P > 0.05). Curcumin plus piperine might be have positive effect on serum IgE levels with no significant changes on serum IL-10 and IL-12 in healthy young women with PMS and PD. Studies with higher doses and longer durations of treatment with curcumin are required to confirm these findings. In light of increasing research evidence on the molecular mechanisms of allergic diseases, the crucial roles of innate and acquired immunity in the disease’s pathogenesis have been well highlighted. In this respect, much attention has been paid to the modulation of unregulated and unabated inflammatory responses aiming to suppress pathologic immune responses in treating allergic diseases. One of the most important natural compounds with a high potency of immune modulation is curcumin, an active polyphenol compound derived from turmeric, Curcuma longa L, Curcumin’s immunomodulatory action mainly arises from its interactions with an extensive collection of immune cells such as mast cells, eosinophils, epithelial cells, basophils, neutrophils, and lymphocytes. Up to now, there has been no detailed investigation of curcumin’s immunomodulatory actions in allergic diseases. So, the present review study aims to prepare an overview of the immunomodulatory effects of curcumin on the pathologic innate immune responses and dysregulated functions of T helper (T H ) subtypes, including T H 1, T H 2, T H 17, and regulator T cells (Tregs) by gathering evidence from several studies of In-vitro and In-vivo, As the second aim of the present review, we also discuss some novel strategies to overcome the limitation of curcumin in clinical use. Finally, this review also assesses the therapeutic potential of curcumin regarding its immunomodulatory actions in allergic diseases. Curcumin (CUR), demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC) are the main components of turmeric that commonly used to treat neuropathic pain (NP). However, the mechanism of the therapy is not sufficiently clarified. Herein, network pharmacology, molecular docking and molecular dynamics (MD) approaches were used to investigate the mechanism of curcuminoids for NP treatment. Active targets of curcuminoids were obtained from the Swiss Target database, and NP-related targets were retrieved from GeneCards, OMIM, Drugbank and TTD databases. A protein-protein interaction (PPI) network was built to screen the core targets. Furthermore, DAVID was used for GO and KEGG pathway enrichment analyses. Interactions between potential targets and curcuminoids were assessed by molecular docking and the MD simulations were run for 100ns to validate the docking results on the top six complexes. CUR, DMC, and BDMC had 100, 99 and 100 targets respectively. After overlapping with NP there were 33, 33 and 31 targets respectively. PPI network analysis of TOP 10 core targets, TNF, GSK3β were common targets of curcuminoids. Molecular docking and MD results indicated that curcuminoids bind strongly with the core targets. The GO and KEGG showed that curcuminoids regulated nitrogen metabolism, the serotonergic synapse and ErbB signaling pathway to alleviate NP. Furthermore, specific targets in these three compounds were also analysed at the same time. This study systematically explored and compared the anti-NP mechanism of curcuminoids, providing a novel perspective for their utilization. Cow milk allergy is one of the most prevalent food allergies worldwide, particularly in infants and children. To the best of our knowledge, minimal research exists concerning the antigenicity of cow milk (CM). This study was performed to evaluate the allergenicity of enzymatically hydrolyzed cow milk (HM) in a BALB/c mouse model. The mice were randomly divided into 5 groups (n = 12/group), which were sensitized with phosphate-buffered saline, CM, and HM (Alcalase-, or Protamex-, or Flavorzyme-treated cow milk; Novo Nordisk; AT, PT, FT, respectively), respectively, using cholera toxin as adjuvant on d 0, 7, 14, 21. On d 28, the test mice were orally challenged with phosphate-buffered saline, CM, and HM (AT, PT, or FT) alone. Anaphylactic symptoms were monitored in the mice. Antibody, cytokine, histamine, and mouse mast cell protease-1 (mMCP-1) levels were measured using enzyme-linked immunosorbent assays. In addition, the numbers of T helper (Th)1 and Th2 cells, as well as the proportions of CD4 + CD25 + Foxp3 + Treg cells, in mouse spleens were detected using flow cytometry. Statistical significance was determined by one-way ANOVA. The results revealed significant differences between CM- and HM-challenged mice. Among these, the clinical scores of HM-challenged mice (AT, 1.50; PT, 2.00; FT, 1.92) were lower than those of CM-challenged mice (positive control, 2.83), but body weight and temperature of HM-challenged mice were higher than those of CM-challenged mice. In addition, significant reductions of allergen-specific IgE, IgG, histamine, and mMCP-1 were showed in HM-challenged mice, especially for histamine, ranging from 171.42 ng/mL to 214.94 ng/mL. Remarkable reductions of IL-4, IL-5, and IL-13 levels, as well as elevations of interferon-γ and IL-10 levels in the spleens of HM-challenged mice were also detected. Moreover, the number of Th2 cells decreased in the HM-challenged mice, to 2.36% (AT), 1.79% (PT), and 4.03% (FT), respectively, whereas the numbers of Th1 cells (AT, 6.30%; PT, 6.70%; FT, 6.56%) and the proportions of CD4 + CD25 + Foxp3 + Tregs (AT, 8.86%; PT, 9.21%; FT, 9.16%) increased significantly. Our findings indicate that exposure to HM was sufficient to induce a shift toward a Th1 response, thereby reducing potential allergenicity. Importantly, these results will lay a theoretical foundation for the development of hypoallergenic CM products. Cross-cultural comparison of plants used during lactation and the postpartum period offers insight into a largely overlooked area of ethnopharmacological research. Potential roles of phytochemicals in emerging models of interaction among immunity, inflammation, microbiome and nervous system effects on perinatal development have relevance for the life-long health of individuals and of populations in both traditional and contemporary contexts. Delineate and interpret patterns of traditional and contemporary global use of medicinal plants ingested by mothers during the postpartum period relative to phytochemical activity on immune development and gastrointestinal microbiome of breastfed infants, and on maternal health. Published reviews and surveys on galactagogues and postpartum recovery practices plus ethnobotanical studies from around the world were used to identify and rank plants, and ascertain regional use patterns. Scientific literature for 20 most-cited plants based on frequency of publication was assessed for antimicrobial, antioxidant, anti-inflammatory, immunomodulatory, antidepressant, analgesic, galactagogic and safety properties. From compilation of 4418 use reports related to 1948 species, 105 plant taxa were recorded ≥7 times, with the most frequently cited species, Foeniculum vulgare, Trigonella foenum-graecum, Pimpinella anisum, Euphorbia hirta and Asparagus racemosus, 81, 64, 42, 40 and 38 times, respectively. Species and use vary globally, illustrated by the pattern of aromatic plants of culinary importance versus latex-producing plants utilized in North Africa/Middle East and Sub-Saharan Africa with opposing predominance. For 18/20 of the plants a risk/benefit perspective supports assessment that positive immunomodulation and related potential exceed any safety concerns. Published evidence does not support a lactation-enhancing effect for nearly all the most-cited plants while antidepressant data for the majority of plants are predominately limited to animal studies. Within a biocultural context traditional postpartum plant use serves adaptive functions for the mother-infant dyad and contributes phytochemicals absent in most contemporary diets and patterns of ingestion, with potential impacts on allergic, inflammatory and other conditions. Polyphenolics and other phytochemicals are widely immunologically active, present in breast milk and predominately non-toxic. Systematic analysis of phytochemicals in human milk, infant lumen and plasma, and immunomodulatory studies that differentiate maternal ingestion during lactation from pregnancy, are needed. Potential herb-drug interaction and other adverse effects should remain central to obstetric advising, but unless a plant is specifically shown as harmful, considering potential contributions to health of individuals and populations, blanket advisories against postpartum herbal use during lactation appear empirically unwarranted,

Food allergy is an adverse immune response to dietary proteins. Hydrolysates are frequently used for children with milk allergy. However, hydrolysates effects afterwards are poorly studied. The aim of this study was to investigate the immunological consequences of hydrolyzed whey protein in allergic mice. For that, we developed a novel model of food allergy in BALB/c mice sensitized with alum-adsorbed β-lactoglobulin. These mice were orally challenged with either whey protein or whey hydrolysate. Whey-challenged mice had elevated levels of specific IgE and lost weight. They also presented gut inflammation, enhanced levels of SIgA and IL-5 as well as decreased production of IL-4 and IL-10 in the intestinal mucosa. Conversely, mice challenged with hydrolyzate maintained normal levels of IgE, IL-4 and IL-5 and showed no sign of gut inflammation probably due to increased IL-12 production in the gut. Thus, consumption of hydrolysate prevented the development of clinical signs of food allergy in mice. Curcumin has commonly been used for the treatment of various allergic diseases. However, its precise anti-allergic rhinitis effect and mechanism remain unknown. In the present study, the effect of curcumin on allergic responses in ovalbumin (OVA)-induced allergic rhinitis mouse was investigated. We explored the effect of curcumin on the release of allergic inflammatory mediators, such as histamine, OVA-specific IgE, and inflammatory cytokines. Also, we found that curcumin improved rhinitis symptoms, inhibited the histopathological changes of nasal mucosa, and decreased the serum levels of histamine, OVA-specific IgE and TNF-α in OVA-induced allergic rhinitis mice. In addition, curcumin suppressed the production of inflammatory cytokines, such as TNF-α, IL-1β, IL-6 and IL-8. Moreover, curcumin significantly inhibited PMA-induced p-ERK, p-p38, p-JNK, p-Iκ-Bα and NF-κB. These findings suggest that curcumin has an anti-allergic effect through modulating mast cell-mediated allergic responses in allergic rhinitis, at least partly by inhibiting MAPK/NF-κB pathway. Curcumin, phytochemical present in turmeric, rhizome of Curcuma longa, a known anti-inflammatory molecule with variety of pharmacological activities is found effective in murine model of chronic asthma characterized by structural alterations and airway remodeling. Here, we have investigated the effects of intranasal curcumin in chronic asthma where animals were exposed to allergen for longer time. In the present study Balb/c mice were sensitized by an intraperitoneal injection of ovalbumin (OVA) and subsequently challenged with 2% OVA in aerosol twice a week for five consecutive weeks. Intranasal curcumin (5 mg/kg) was administered from days 21 to 55, an hour before every nebulization and inflammatory cells recruitment, levels of IgE, EPO, IL-4 and IL-5 were found suppressed in bronchoalveolar lavage fluid (BALF). Intranasal curcumin administration prevented accumulation of inflammatory cells to the airways, structural alterations and remodeling associated with chronic asthma like peribronchial and airway smooth muscle thickening, sloughing off of the epithelial lining and mucus secretion in ovalbumin induced murine model of chronic asthma. Food allergy is a severe human disease with imminent risk of life. Cissampelos sympodialis (Menispermaceae) is a native Brazilian plant used in Brazilian folk medicine for the treatment of respiratory allergies. In this study the experimental model of food allergy induced by ovalbumin (OVA) was used to determine whether the alcoholic extract of the plant (AFL) and its alkaloids match a therapeutic approach for this disease. Animal weight, diarrhea, OVA-specific IgE levels, inflammatory cell and cytokine profiles, mucus production and proportion of T cells on the mesenteric lymph node (MLN) were evaluated. Warifteine (W) or methyl-warifteine (MW) alkaloids slightly improve diarrhea score independently of AFL and all treatments decreased the OVA-specific IgE levels. Stimulated mesenteric lymph node (MLN) cells in the presence of the alkaloids diminished the IL-12p70 levels independently of IFN-γ or IL-13 secretion. The alkaloids increased the number of Treg cells on MLN and reduced the number of eosinophils and mast cells as well as mucus production in the gut. Therefore, the alkaloids modulate the immune response in food allergy by increasing regulatory T cells in MLN independently of Th1 or Th2 profiles. In our mouse model, gastric acid-suppression is associated with antigen-specific IgE and anaphylaxis development. We repeatedly observed non-responder animals protected from food allergy. Here, we aimed to analyse reasons for this protection. Ten out of 64 mice, subjected to oral ovalbumin (OVA) immunizations under gastric acid-suppression, were non-responders without OVA-specific IgE or IgG1 elevation, indicating protection from allergy. In these non-responders, allergen challenges confirmed reduced antigen uptake and lack of anaphylactic symptoms, while in allergic mice high levels of mouse mast-cell protease-1 and a body temperature reduction, indicative for anaphylaxis, were determined. Upon OVA stimulation, significantly lower IL-4, IL-5, IL-10 and IL-13 levels were detected in non-responders, while IL-22 was significantly higher. Comparison of fecal microbiota revealed differences of bacterial communities on single bacterial Operational-Taxonomic-Unit level between the groups, indicating protection from food allergy being associated with a distinct microbiota composition in a non-responding phenotype in this mouse model. Alginate is a dietary polysaccharide that exerts antioxidative, immunomodulatory and anti-allergic effects. In this study, the effects of alginate on the secondary structure of ovalbumin (OVA) in vitro and on the regulation of OVA-induced gut microbiota disorders in vivo were investigated. First, the interactions between OVA and alginate were studied by multiple spectroscopic methods, which showed that alginate could change the secondary structure of OVA. Then, the regulation of allergic diarrhoea by alginate was evaluated in OVA-sensitized mice, which demonstrated that alginate could attenuate allergic diarrhoea and duodenal morphological damage. Additionally, when diarrhoea symptoms were ameliorated by alginate, the richness and diversity of the gut microbiota could be partially restored, and the relative abundances of Alloprevotella, Bacteroides, Parabacteroides and Rikenellaceae_RC9_gut_group showed recovery trends. Therefore, alginate could improve OVA-induced gut microbiota disorder, and alginate could be used as a potential agent for intestinal protection in the food or pharmaceutical industry.

: Turmeric (Curcuma longa) attenuates food allergy symptoms by regulating type 1/type 2 helper T cells (Th1/Th2) balance in a mouse model of food allergy

Does green tea reduce IgE levels?

Green Tea (Camelia Sinensis) Suppresses B Cell Production Of IgE Without Inducing Apoptosis. RATIONALE: Green tea (Camelia sinensis) has been shown to possess biological properties that are antioxidative and antimutagenic. Recent studies have demonstrated beneficial effects in inflammatory allergy.

Can stress increase IgE levels?

Discussion – Anxiety heightened the magnitude of SPT wheals following the stressor. As anxiety increased the SPT responses increased after the stressor, compared to a slight decrease following the control task. Anxiety also enhanced the effects of stress on late phase responses; indeed, even skin tests performed the day after the stressor reflected the continuing impact of the event among the more anxious participants.

1. The inflammation that occurs during late phase allergic responses is thought to promote “priming” such that the dose of allergen required to elicit subsequent acute responses substantially decreases ( Skoner, 2001 ).
2. Moreover, priming can lead to hyperresponsiveness to other allergens as well as to nonspecific irritant triggers such as smoke, exercise, and noxious odors; these effects can be particularly troublesome, because the nonspecific triggers can then promote additional clinical symptoms even after allergen exposure has ended ( Skoner, 2001 ).

Our data suggest that both stress and anxiety function to enhance late phase SPT responses as well as some aspects of inflammation; accordingly, stress and anxiety may also promote priming and hyperresponsiveness to irritant triggers as well as to other allergens.

1. Late phase symptoms include postnasal drainage and nasal congestion, fatigue, drowsiness, impairments in concentration, irritability, and disrupted sleep, and these symptoms interfere with work and school performance as well as disrupting social interactions ( Bender, 2005 ).
2. The evidence that stress and anxiety amplify late phase SPT responses has potential clinical significance for AR patients.

While the immediate phase symptoms can be readily treated or even prevented in most patients with the use of antihistamines, late phase responses are poorly responsive to antihistamine treatment ( Marshall, 2004a ). Our data suggest that the highly anxious patient, after exposure to an acute stressor, can have increased immediate as well as late phase responses that would be less responsive to first line therapies such as antihistamines.

If similar immune changes occur in other inflammatory diseases with acute stress superimposed on chronic anxiety, this could account (at least in part) for the known association between stress and adverse clinical reactions such as asthma exacerbation, autoimmune disease exacerbation and even acute cardiovascular events.

AR symptoms can substantially disrupt sleep, enhancing AR-associated fatigue. Importantly, sleep deprivation can exacerbate allergic responses in turn; one study showed that AR patients had substantially greater wheal responses and IgE production following a night of sleep deprivation than after a rested baseline ( Kimata, 2002 ).

Furthermore, in our study more anxious participants reported poorer sleep than those who were less anxious, an expected finding because poorer sleep is a common anxiety symptom. Thus, sleep disruption provides another important avenue through which stress and anxiety can intensify AR symptoms. Compared to those who were less anxious, more anxious participants felt more threatened by the speech stressor; afterwards they felt less in control and more helpless, and their PBLs had greater Con A-stimulated IL-6 production compared to the control condition.

Moreover, having a late phase response was associated with higher IL-6 production. Relatedly, in another study asthmatic children who reported lower levels of perceived control had higher levels of asthma-relevant Th2 stimulated cytokine production, including IL-4, IL-5, and IL-13 ( Griffin and Chen, 2006 ).

Stressors that engender feelings of helplessness and lack of control augment and prolong psychological and physiological stress responses ( Breier et al., 1987b ; Brosschot et al., 2005 ); anxious individuals who worry more about negative outcomes are particularly susceptible because they have stronger anticipatory responses as well as slower recovery than those who are less anxious ( Brosschot et al., 2005 ).

The probability of experiencing a late phase skin increased with the level of anxiety; indeed, in contrast to the immediate wheal diameter which was only different immediately post task, the late phase response was related to anxiety levels over the entire period of the experiment.

• This is not surprising given the increased inflammatory milieu associated with a late phase allergic response that is predominantly TH2 in nature, and the fact that TH2 predominance is enhanced by stress ( Agarwal and Marshall, 1998 ; Marshall et al., 1998 ).
• The fact that neither glucocorticoid resistance nor plasma IL-6 levels were related to either anxiety or stress is likely a function of the timing of the samples; the blood samples for these assays were drawn 45 minutes after the stressor.

Stress- and distress-related differences in these assays are amplified 1.5-2 hours after stressors like the TSST ( Pace et al., 2006 ; Steptoe et al., 2007 ). One limitation of our study is the relatively low level of anxiety symptoms in our sample, which were well below those of clinical anxiety disorders.

Indeed, in samples of AR patients seeking allergy treatment, the mean STAI anxiety scores were higher than those of our participants ( Addolorato et al., 1999 ; Annesi-Maesano et al., 2006 ), consistent with the over-representation of clinical anxiety disorders in AR populations ( Cuffel et al., 1999 ).

Accordingly, our data are likely to underestimate the actual contribution of anxiety to AR symptoms, particularly in patients with clinically active disease. In fact, even in our relatively small sample in which anxiety was in the normative range, we found that participants who were more anxious showed larger increases in negative affect than less anxious participants; this finding may be particularly relevant given the well-documented association between depression and allergic disorders ( Goodwin et al., 2006 ; Kovacs et al., 2003 ; Meggs et al., 2001 ; Wamboldt et al., 2000 ).

1. We did not conduct formal mental health assessments of subjects, and we limited exclusionary criteria in this regard to the absence of current psychotropic medications, so we do not know if any of our subjects had experienced syndromal mood disorders.
2. This study did not specifically assess the effects of an acute stressor on clinical symptoms.

This was by design because clinical symptomatology can vary between individuals as well as within an individual from day to day based upon many factors in addition to their level of stress. By doing SPT measurements in participants who were currently asymptomatic, we avoided the complication of interpreting subjective clinical symptoms such as stuffiness or congestion in the context of anxiety and stress responses.

1. SPTs can be a reliable surrogate; both total and specific IgE and allergic symptomatology correlate with reactivity to skin tests ( Brown et al., 1979 ); indeed, correspondence between skin tests and inhalation challenge varies from 60-90% ( Bernstein and Storms, 1995 ).
2. Moreover, our data complement and extend the finding that the stress of academic examinations can augment allergic responses to inhaled allergens in asthmatics ( Liu et al., 2002 ).

The allergic patient provides one of the most relevant and translatable models for studying the effects of various forms of stress, both acute and chronic, on complex immunoregulatory mechanisms ( Marshall and Roy, 2007 ). The mast cell is a fundamental component of innate host defense, being able to respond to challenge in a matter of minutes.

Its activity is made much more efficient by arming with allergen specific IgE via high affinity receptors (F c εR1). Both IgE and its receptor are produced under the control of TH2 cytokines such as IL-4. Stress has been associated with elevated IgE levels ( Buske-Kirschbaum et al., 2004 ; Wright et al., 2004 ), and our SPT responses provided evidence of the ability of stress and anxiety to modulate allergen-specific IgE response.

Of note, elevated IgE levels have been shown to be independent risk factors for allergic conditions such as asthma and atopic dermatitis ( Wright, 2005 ), both of which are more prevalent in patients with underlying AR. However, it is the late phase response that is associated with higher morbidity in virtually all allergic syndromes including those of the nose (AR), lungs (asthma) and skin (atopic dermatitis).

• AR has a substantial public health impact; it is the fifth most common chronic disease, affecting 10-30% of adults and up to 40% of children in the United States, and the prevalence of AR appears to be increasing worldwide ( Skoner, 2001 ).
• Estimates of the medical costs associated with AR are $3.4 billion ($2.3 billion in medications and $1.1 billion in physician billings), not including the 3.5 million workdays and 154 million in wages lost because of seasonal nasal allergies ( Storms et al., 1997 ).

However, the public health burden is actually much greater than suggested by these numbers, because AR is associated with a number of other allergic diseases, including asthma rhinosinusitis; survey data suggest that 38% of AR patients have coexisting asthma, and 78% of asthma patients have AR ( Nathan, 2007 ).

Improvement in AR can promote positive changes in asthma; conversely, deterioration in AR can worsen asthma ( Nathan, 2007 ). Thus, by enhancing and prolonging allergic responses, stress and anxiety substantially impact public health. The data also have implications for clinical practice. Indeed, these results should alert practitioners and patients alike to the adverse effects of stress and anxiety on allergic reactions in the nose, chest, skin and other organs that may seemingly resolve within a few minutes to hours after starting, but may reappear the next day when least expected.

The evidence that anxiety fuels stress-related changes suggests that more systematic assessment of allergic patients for comorbid anxiety disorders might be in order. Indeed, management-based interventions (psychological, pharmacological) that target various forms of stress could be rapidly (minutes to hours) evaluated for their clinical potential by testing the impact of a given intervention on the immediate and late phase skin test responses.

What autoimmune causes high IgE?

Definition of Hyper IgE Syndrome – HIES is a rare primary immunodeficiency characterized by recurrent eczema, skin abscesses, lung infections, eosinophilia and high serum levels of IgE. Two form of HIES have been described, including an autosomal dominant (AD, or type 1) and an autosomal recessive (AR, or type 2) form.

What disease has high IgE levels?

Topic Resources Hyper-IgE syndrome is a hereditary immunodeficiency disorder characterized by recurring boils, sinus and lung infections, and a severe rash that appear during infancy. Levels of immunoglobulin E (IgE) are very high.

In infants with hyper-IgE syndrome, abscesses form in the skin, joints, lungs, or other organs. Blood tests can confirm the diagnosis. Treatment involves giving antibiotics to prevent or treat infections, creams or drugs to relieve the rash, and drugs that modify the immune system.

How hyper-IgE is inherited depends on which gene is affected. Both forms cause similar symptoms. An itchy rash develops. Bones are weak, resulting in many fractures. Facial features may be coarse. Loss of baby teeth is delayed. Life span depends on the severity of the lung infections.

Blood tests to measure IgE levels Sometimes genetic testing

Hyper-IgE syndrome is suspected when boils and pneumonia develop frequently in infants. The diagnosis is confirmed by blood tests that detect a high level of IgE. Genetic tests can be done to check for the abnormal genes. Antibiotics, usually trimethoprim /sulfamethoxazole, are given continuously to prevent staphylococcal infections.

1. The rash is treated with moisturizing creams, antihistamines, and, if infection is likely, antibiotics.
2. Respiratory infections are treated with antibiotics.
3. Certain drugs that modify the immune system, such as interferon gamma, are sometimes helpful.
4. The following English-language resource may be useful.

Please note that THE MANUAL is not responsible for the content of this resource. NOTE: This is the Consumer Version. DOCTORS: VIEW PROFESSIONAL VERSION VIEW PROFESSIONAL VERSION Copyright © 2023 Merck & Co., Inc., Rahway, NJ, USA and its affiliates. All rights reserved.

What is the problem if IgE levels are high?

What Is an Immunoglobulin E Test? – An immunoglobulin E (IgE) test measures the level of IgE, a type of antibody. Antibodies (also called immunoglobulins) are proteins the immune system makes to recognize and get rid of germs, The blood usually has small amounts of IgE antibodies.

Can inflammation cause high IgE?

Skin inflammation increases IgE levels locally and systemically – Both basophils and mast cells carry a high number of FcεRI receptors, which are usually occupied with IgE ( Lawrence et al., 2017 ). Consistent with this, a horizontal view of resting healthy murine skin revealed that large amounts of IgE was normally present in the tissue ( Figure 1a ) despite very low levels in serum ( Figure 1b–d ).

IgE in resting skin was mainly found on cells around the hair-follicles ( Figure 1a ). Topical exposure to agents that induce skin inflammation, such as 12- O -tetradecanoylphorbol-13-acetate (TPA, a protein kinase C activator) ( Figure 1b ), MC903 (a vitamin D3 analogue commonly used to induce atopic dermatitis-like inflammation) ( Figure 1c ) and R848 (resiquimod, a toll-like receptor seven agonist commonly used to induce psoriasis-like inflammation) ( Figure 1d ), significantly enhanced the circulating levels of IgE compared to those in untreated or vehicle-treated animals.

Enhancement of serum IgE was dependent on topical exposure: intravenous (i.v.) or intraperitoneal (i.p.) administration did not trigger the same effect, as shown by R848 exposure ( Figure 1d ). Skin inflammation increases IgE levels locally and systemically. ( a ) Representative image of IgE staining (red) in healthy dermal skin. Scale = 50 μm. The image is representative of tile-scans from healthy untreated (UT) dermal sheets of five independent mice. ( b–d ) ELISA of IgE in serum of UT wildtype (WT) BALB/c mice and mice treated on the dorsal ear skin with ( b ) 2.5 nM TPA 2x a week for 2 weeks or vehicle control (ethanol) (n = 8), ( c ) 1 nM MC903 5x a week for 2 weeks or vehicle control (ethanol) (n = 5) or ( d ) 100 μg R848 3x a week for 2 weeks or similarly i.v. or i.p. (n = 4). Data are expressed as means ± SEM. ( e, f ) Fluorescence-assisted cell sorting (FACS) analysis of IgE-secreting plasma cells in the skin draining LNs of UT WT mice and mice exposed topically to TPA on the dorsal side of the ears 2x a week for 2 weeks. ( e ) Representative plots of plasma cells gated as FSC hi CD95 + CD138 + cells, and with intracellular IgE staining to show isotype switching. ( f ) Enumeration of IgE + plasma cells in skin draining LN (n = 4). ( g ) Representative images of IgE staining (green) in UT and TPA treated whole skin. Nuclei in blue. Scale = 100 μm. Images are representative of tile-scans from ear cross-sections from six independent mice. ( h, i ) FACS analysis of IgE-bearing cells in whole naïve UT skin and in TPA-treated skin (TPA 2x a week for 2 weeks). ( h ) Representative plots of IgE-bearing mast cells (green) and basophils (blue) 48 hr after last TPA exposure. ( i ) Enumeration of IgE-bearing mast cells and basophils at the indicated time points after topical TPA. Mast cells were defined as CD45 hi cKit + IgE + CD41 – and basophils as CD45 lo cKit – IgE + CD41 + (n = 5). One-way ANOVA multiple comparison ( b, d ) and two-tailed Student’s t-test for unpaired data ( c, f ) were used to test for statistical difference. **p<0.01 and ****p<0.0001. IP, intraperitoneal; IV, intravenous; UT, untreated. The increase in serum IgE was accompanied by an increase in the number of IgE-secreting plasma cells in the skin-draining lymph nodes (LNs) ( Figure 1e,f ). IgE levels were also increased locally in the skin following topical TPA treatment ( Figure 1g ), but most notably the cells carrying the IgE switched from being predominantly mast cells in resting untreated skin to mainly basophils in TPA-treated inflamed skin ( Figure 1h,i ).24 hr after cessation of TPA treatment, only a few mast cells remained in the skin, while IgE-bearing basophils accounted for ~2% of total CD45 + leukocytes. Basophil numbers further increased at 48 hr after cessation of TPA treatment and then declined as the inflammation subsided, while mast cells returned to the skin ( Figure 1i ). Thus, untreated resting skin contains high levels of IgE antibodies that are predominately carried on mast cells. Skin inflammation increases IgE levels locally and systemically, and IgE antibodies in inflamed skin are mainly carried on basophils.

Can probiotics reduce IgE?

Human Studies – A meta-analysis of randomized controlled trials (RCTs) showed that supplemented with Lactobacillus rhamnosus GG reduced the incidence of asthma, and probiotic supplementation before and after delivery may play an important strategic role in asthma prevention ( 113 ).

However, a randomized, controlled, double-blind study of 159 newborns found that supplementation with Lactobacillus rhamnosus GG for the first 6 months of life seems not to prevent the development of asthma at age two ( 114 ). In addition, using of probiotics for asthma early in life demonstrated a significant reduction intotal IgE and atopic allergy in a meta-analysis ( 115 ).

Moreover, patients with asthma have elevated blood levels of TNF-α, interferon-δ, and IL-12. Chen et al. found there was a positive effect on clinical symptoms and cytokine levels in asthmatic children 6 to 12 years old on daily doses of Lactobacillus for 2 months ( 39 ). Figure 1, Effect of probiotics on allergic asthma. Probiotics protect the homeostasis of the immune system by regulating the Th1 and Th2 balance, reducing the inflammatory response, increasing the number of Tregs, and modulating the gut microbiota. Th1, T helper 1; Th2, T helper 2; AHR, Airway hyperresponsiveness; IgE, Immunoglobulin E; IgA, Immunoglobulin A; IL-4, Interleukin 4; IL-5, Interleukin 5; TGF-β, Transforming growth factor-beta; DCs, Dendritic cells; Tregs, Regulatory T cells; SCFA, Short-chain-fatty acids.

How long does it take for IgE levels to reduce?

Abstract – We present results from clinical studies on plasma infusion done in the late 1970s in patients with hypogammaglobulinemia in which we documented the short half-life of both total and allergen-specific IgE in serum. The development of specific allergic sensitization in the skin of those patients followed by the gradual decrease in sensitization over 50 days was also documented.

1. The data are included here along with a discussion of the existing literature about the half-life of IgE in both the circulation and skin.
2. This rostrum reinterprets the earlier clinical studies in light of new insights and mechanisms that could explain the rapid removal of IgE from the circulation.
3. These mechanisms have clinical implications that relate to the increasing use of anti-IgE mAbs for the treatment of allergic disease.

Keywords: Immunoglobulin, IgE, half-life, metabolism, omalizumab It is generally recognized that the half-life of IgE in serum is short (ie, 2–3 days), whereas the half-life of IgG is much longer (23 days).1 This long half-life of IgG is attributed to the protection of IgG from catabolism by binding to the neonatal Fc receptor (FcRn).2, 3 However, the reason for the shorter half-life of IgE in comparison with other serum immunoglobulins, which also are not protected by FcRn (5–6 days for IgM and IgA), is not clear.

Certainly none of our textbooks includes a coherent explanation of the reasons for the rapid removal of IgE from the circulation.1, 4 – 7 The original studies on the half-life of IgE were carried out in the early 1970s with radiolabeled IgE.1 In those experiments it was difficult to exclude the possibility that the labeling procedure influenced IgE metabolism, although similar results were seen with unlabeled and C 14 -labeled IgE in individual experiments.

In addition, the lack of known specificity of myeloma IgE used in the original studies meant that the presence of IgE could not be detected or monitored by using skin testing. Here we present results from clinical studies on plasma infusion done in the late 1970s in patients with hypogammaglobulinemia, in whom we documented the short half-life of both total and allergen-specific IgE in serum.

• The development of specific allergic sensitization in the skin of those patients followed by the gradual decrease in sensitization over 50 days was also documented.
• These results were only reported in abstract form because we could not adequately explain where the serum IgE went or how it was catabolized.

The data are included here along with a discussion of the existing literature about the half-life of IgE in both the circulation and the skin.8 This rostrum reinterprets the earlier clinical studies in light of newer developments in the field that could explain the rapid removal of IgE from the circulation.

Do antihistamines lower IgE levels?

Phytochemicals in Cardiovascular and Respiratory Diseases: Evidence in Oxidative Stress and Inflammation – View this Special Issue Research Article | Open Access Academic Editor: Ada Popolo Received 17 Feb 2018 Revised 13 Apr 2018 Accepted 15 May 2018 Published 12 Jun 2018 The aim of the study was the analysis of adhesion molecules’ profile (ICAM-1, VCAM-1, and E-selectin) in patients with allergic rhinitis and the influence of H1 antihistamines on those markers.

Seventy-nine patients with persistent allergic rhinitis (PAR) and 30 healthy volunteers were included in the study. The patients with PAR were treated with desloratadine 5 mg/day or levocetirizine 5 mg/day for 4 weeks. The clinical (rhinitis symptoms and total symptoms score (TSS), type of sensitization) and biological evaluation (total IgE, eosinophils, ICAM-1, VCAM-1, and E-selectin) as well as fractionate nitric oxide in exhaled air (FeNO) measurement was performed before and after treatment.

The plasmatic levels of ICAM-1, VCAM-1, total IgE, and eosinophils and FeNO were significantly increased in patients with PAR compared to healthy volunteers. H1 antihistamines significantly improved TSS, with no differences between the investigated drugs.

There was a significant decrease of eosinophils, total IgE, and FeNO after treatment. H1 antihistamines significantly decreased the plasmatic levels of ICAM-1 and E-selectin but not VCAM-1 compared to basal values. There is no difference between levocetirizine and desloratadine in the reduction of CAMs.

A systemic inflammation characterized by increased levels of CAMs is present in patients with PAR. H1 antihistamines improve symptoms and reduce CAMs and FeNO levels after 1 month of treatment. H1 antihistamines might reduce the systemic inflammation which could be responsible to asthma occurrence in patients with PAR.

Which foods increase IgE levels?

IgE-mediated food allergies cause your child’s immune system to react abnormally when exposed to one or more specific foods such as milk, egg, wheat or nuts. Children with this type of food allergy will react quickly — within a few minutes to a few hours.

Milk Egg Soy Wheat Peanut Tree nuts Fish Shellfish

All of these foods can trigger anaphylaxis (a severe, whole-body allergic reaction) in patients who are allergic. Food allergies are common: 5 percent of children under the age of five have a food allergy and roughly 4 percent of adolescents and adults have a food allergy.

The prevalence of food allergies does seem to be increasing. Researchers at The Children’s Hospital of Philadelphia are evaluating the genetics of food allergy and possible reasons for the increase in all allergic conditions. Researchers believe many factors may play a role in food allergy development including maternal diet during pregnancy, timing of food introduction, and breastfeeding status.

How to fight allergies naturally, histamine and antihistamine food

If you have an “allergic family” — one that includes family members with asthma, environmental allergies and eczema — your child has an increased risk for allergy. When IgE is working properly, it identifies triggers — such as parasites or other items that could be harmful to the body — and tells the body to release histamine.

1. Histamine causes symptoms such as cough, wheeze and hives.
2. However, IgE can sometimes react to normal proteins, causing your child’s body to react to a specific food protein or proteins.
3. Once a food is eaten, the protein is absorbed during digestion and enters the bloodstream.
4. That food will cause symptoms throughout the body because of IgE.

For example, if your child has an IgE-mediated allergy to the protein in milk, he may experience symptoms in the skin (hives), stomach (vomiting), lungs (coughing, wheezing), and circulatory system (decreasing blood pressure). When your child has a food allergy, her body’s IgE antibodies identify that specific food as an invader and can produce symptoms in multiple areas of the body, including:

Skin: “hives” (red blotches or welts that itch), mild to severe swelling Eyes: tearing, redness, itch Nose: clear discharge, itch, congestion Mouth: itch, lip swelling, tongue swelling Throat: tightness, trouble speaking, trouble inhaling Lungs: shortness of breath, rapid breathing, cough, wheeze Stomach: repeated vomiting, nausea, abdominal pain, diarrhea (usually later) Heart and circulation: weak pulse, loss of consciousness Brain: anxiety, agitation, loss of consciousness

Allergic reactions can be scary, but noticing symptoms early can help your child get proper treatment. Reactions to food can be different every time. Your child’s reaction can depend on a variety of factors including the amount of food eaten, uncontrolled asthma, and illness.

Your child may have had a reaction to a food which led to an evaluation by an allergist Your child may have had a flare of eczema, which led to concerns about a food allergy You may have discussed concerns about your child with her pediatrician, who recommended consultation with a specialist

When you meet with allergy specialists at The Children’s Hospital of Philadelphia, we will discuss your child’s food reaction history, as well as get a detailed medical and family history. Based on your child’s history and findings, our allergy specialists may recommend testing.

How long does it take for IgE levels to reduce?

Abstract – We present results from clinical studies on plasma infusion done in the late 1970s in patients with hypogammaglobulinemia in which we documented the short half-life of both total and allergen-specific IgE in serum. The development of specific allergic sensitization in the skin of those patients followed by the gradual decrease in sensitization over 50 days was also documented.

The data are included here along with a discussion of the existing literature about the half-life of IgE in both the circulation and skin. This rostrum reinterprets the earlier clinical studies in light of new insights and mechanisms that could explain the rapid removal of IgE from the circulation. These mechanisms have clinical implications that relate to the increasing use of anti-IgE mAbs for the treatment of allergic disease.

Keywords: Immunoglobulin, IgE, half-life, metabolism, omalizumab It is generally recognized that the half-life of IgE in serum is short (ie, 2–3 days), whereas the half-life of IgG is much longer (23 days).1 This long half-life of IgG is attributed to the protection of IgG from catabolism by binding to the neonatal Fc receptor (FcRn).2, 3 However, the reason for the shorter half-life of IgE in comparison with other serum immunoglobulins, which also are not protected by FcRn (5–6 days for IgM and IgA), is not clear.

Certainly none of our textbooks includes a coherent explanation of the reasons for the rapid removal of IgE from the circulation.1, 4 – 7 The original studies on the half-life of IgE were carried out in the early 1970s with radiolabeled IgE.1 In those experiments it was difficult to exclude the possibility that the labeling procedure influenced IgE metabolism, although similar results were seen with unlabeled and C 14 -labeled IgE in individual experiments.

In addition, the lack of known specificity of myeloma IgE used in the original studies meant that the presence of IgE could not be detected or monitored by using skin testing. Here we present results from clinical studies on plasma infusion done in the late 1970s in patients with hypogammaglobulinemia, in whom we documented the short half-life of both total and allergen-specific IgE in serum.

The development of specific allergic sensitization in the skin of those patients followed by the gradual decrease in sensitization over 50 days was also documented. These results were only reported in abstract form because we could not adequately explain where the serum IgE went or how it was catabolized.

The data are included here along with a discussion of the existing literature about the half-life of IgE in both the circulation and the skin.8 This rostrum reinterprets the earlier clinical studies in light of newer developments in the field that could explain the rapid removal of IgE from the circulation.

Can exercise lower IgE levels?

It has also been suggested that moderate-intensity physical training may induce a decrease in both total and allergen-specific IgE levels.

Can turmeric reduce IgE level?

Turmeric (Curcuma longa) attenuates food allergy symptoms by regulating type 1/type 2 helper T cells (Th1/Th2) balance in a mouse model of food allergy , 4 December 2015, Pages 21-29 Turmeric ( ) has traditionally been used to treat pain, fever, allergic and such as,, and dermatitis. In particular, turmeric and its active component,, were effective in ameliorating immune disorders including allergies.

However, the effects of turmeric and curcumin have not yet been tested on, Mice were immunized with intraperitoneal (OVA) and alum. The mice were orally challenged with 50 mg OVA, and treated with turmeric extract (100 mg/kg), curcumin (3 mg/kg or 30 mg/kg) for 16 days. Food allergy symptoms including decreased rectal temperature, diarrhea, and were evaluated.

In addition, cytokines, immunoglobulins, and mouse mast cell protease-1 (mMCP-1) were evaluated using, Turmeric significantly attenuated food allergy symptoms (decreased rectal temperature and anaphylactic response) induced by OVA, but curcumin showed weak improvement.

1. Turmeric also inhibited IgE,, and mMCP-1 levels increased by OVA.
2. Turmeric reduced type 2 helper cell (Th2)-related cytokines and enhanced a Th1-related cytokine.
3. Turmeric ameliorated OVA-induced food allergy by maintaining Th1/Th2 balance.
4. Furthermore, turmeric was confirmed anti-allergic effect through promoting Th1 responses on Th2-dominant immune responses in immunized mice.

Turmeric significantly ameliorated food allergic symptoms in a mouse model of food allergy. The turmeric as an anti-allergic agent showed immune regulatory effects through maintaining Th1/Th2 immune balance, whereas curcumin appeared immune suppressive effects.

Therefore, we suggest that administration of turmeric including various components may be useful to ameliorate Th2-mediated allergic disorders such as food allergy, atopic dermatitis, and asthma. Allergic reactions occur when the immune system overreacts to normally harmless substances in the environment.

This hypersensitivity occurs in various forms including atopic dermatitis, asthma, allergic rhinitis, and food allergies. The incidence of allergic reactions has been increasing every year. In particular, food allergies have been estimated to affect ~6% of children and ~4% of the adult population (Sampson, 1976, Venter et al., 2008).

1. To treat or prevent allergic disorders, many studies are currently in progress, and many drugs have been developed such as immunosuppressants, antihistamines, and steroids (Wong et al., 2013; Kim et al., 2013; Conen et al., 2013).
2. Although these drugs are effective, when taken for long periods, these drugs may have adverse effects such as growth retardation, diabetes, hypertension, cataracts, and osteoporosis (de Benedictis and Bush, 2012; Elphick and Southern, 2012).

Due to these potential problems, natural products may provide an alternative to effectively treat allergies with fewer adverse effects. The rhizome of Curcuma longa Linn., called turmeric (given the name curry spice by the British), has been widely consumed as a seasoning and used for the treatment of inflammatory disorders in gastrointestinal and respiratory systems in Asian countries such as China, Japan, Korea, and India (Srinivasan, 1953; Gilani et al., 2005).

• Turmeric has been also studied expansively for its pharmacological activities such as antioxidant, anti-inflammatory, anti-cancer, anti-microbial, and neuroprotective effects (Toda et al., 1985; Chandra and Gupta, 1972; Kuttan et al., 1985; Lutomski et al., 1974; Rajakrishnan et al., 1999).
• Curcumin, a main ingredient derived from turmeric, has been also claimed to be an antioxidant and anti-inflammatory agent (Balasubramanyam et al., 2003; Aggarwal et al., 2007).

The immunoregulatory activities of curcumin have been extensively studied since they were first reported in 1999 (Antony et al., 1999). For example, curcumin attenuated allergic airway inflammation by regulating the balance of CD4 + CD25 + regulatory T cells (Tregs) /T-helper (Th) in ovalbumin (OVA) -sensitized mice (Ma et al., 2013).

In allergic disorders, turmeric and curcumin ameliorated allergic rhinitis (Thakare et al., 2013), asthma (Oh et al., 2011), food allergy (Mathias et al., 2013), allergic conjunctivitis (Chung et al., 2012), and allergic contact dermatitis (Thompson and Tan, 2006) through regulation of Th2-, immunoglobulin E (IgE) – and mast cell-mediated immune responses.

However, especially in food allergy, it has not been known whether turmeric and curcumin can attenuate allergic responses to food in a mouse model of food allergy, and also how they regulate. Therefore, we investigated the effects of turmeric and curcumin as a positive control on T cell-mediated immune responses in an OVA-induced mouse model of food allergy.

• RPMI 1640 medium, fetal bovine serum, penicillin-streptomycin, and Dulbecco’s phosphate-buffered saline (D-PBS) were purchased from WelGENE (Daegu, Korea).
• OVA (grade VI), red blood cell lysis buffer, and curcumin were purchased from Sigma-Aldrich (St.
• Louis, MO, USA).
• Turmeric used in this study was purchased from Kyeong-dong Oriental Pharmacy (Seoul, Korea) and identified by Professor Y.

Bu, Department of Herbal Pharmacology, Kyung Hee University. The specimen (KFRI-SL-1005) has been stored at Turmeric extract is traditionally used for the treatment of pain, fever, allergic and inflammatory diseases such as bronchitis, arthritis, and dermatitis.

1. However, the scientific proof for anti-allergic effects of turmeric extract is not clear, especially for food allergy.
2. In this study, we examined the anti-allergenic effects of turmeric extract with curcumin as a positive control in a mouse model of food allergy.
3. Th2 cells producing IL-4, IL-5, and IL-13 play a critical role in the initiation In this study, we investigated anti-allergic effects of turmeric extract and curcumin in a mouse model of food allergy (Fig.1).

We treated mice with 100 mg/kg body weight of turmeric extract by oral gavage because of biological activity of turmeric extract (Ishita et al., 2004). And 3 mg/kg body weight of curcumin administered by oral gavage to mice because turmeric extract contains about 3% curcumin (Tayyem et al., 2006).

Therefore, the turmeric extract and curcumin L groups provided the same In the present study, turmeric extract significantly attenuated OVA-induced food allergic symptoms, whereas curcumin, an active component of turmeric, showed a tendency to reduce allergic symptoms in a mouse model of food allergy.

Turmeric extract regulated immune responses to maintain Th1/Th2 immune balance, although curcumin treatments showed immune suppressive effects. Therefore, the turmeric extract, which includes various active components as well as curcumin, can be used as an The authors have no conflict of interest to declare.

S. Bischoff et al. A.H. Gilani et al. M. Karaman et al. R. Kuttan et al. H. Lee et al. J.H. Lee et al. C. Ma et al. D.O. Moon et al. O. Naksuriya et al. S.W. Oh et al.

K. Reyes-Gordillo et al. S. Sharma et al. S.H. Sicherer et al. Subhashini et al. V.N. Thakare et al. R. Wong et al. B.B. Aggarwal et al. R. Aldini et al. S. Antony et al. M. Balasubramanyam et al. D. Chandra et al. S.H. Chung et al. S. Conen et al. F.M. de Benedictis et al.

This study aimed to explore the underlying mechanism about combined thermal/pressure processing on the allergenicity of shrimp ( Macrobrachium nipponense ). We analysed sensitizing and eliciting capacities, structural changes, gastrointestinal digestion, and mapped linear epitopes. Mice treated with steamed + reverse-pressure sterilized shrimp exhibited lower specific IgE and IgG 1 concentrations, degranulation, vascular permeability, and allergic symptoms than those fed with raw shrimp or steamed shrimp ( p < 0.05). Reduced allergenicity of shrimp using combined thermal/pressure processing was not only associated with protein unfolding and exposure of hydrophobic residues, but also related to disruption of immunodominant linear epitopes (Glu177-Ser188 in tropomyosin, Gln361-Ser366 in β-actin) due to changes in gastrointestinal digestion behavior. Moreover, heat/digested stable epitopes of arginine kinase were located inside its 3D structure, preventing binding with IgE and maintaining hypoallergenicity following combined processing. Thus, steaming and reverse-pressure sterilization might be an efficient low-allergenic food processing method for Macrobrachium nipponense, Premenstrual syndrome (PMS) and primary dysmenorrhea (PD) are common gynecological complications and there is evidence that inflammation may be an important factor in their etiology. There is a relationship between PMS and PD with susceptibility to allergic disorders. We aimed to assess the effect of curcumin co-administered with piperine on serum IL-10, IL-12 and IgE levels in patients with PD and PMS. A sample of 80 patients were recruited to this triple-blind, placebo-controlled clinical trial. Participants were randomly allocated to curcumin (n = 40) and control groups (n = 40). Each participant received one capsule (500 mg of curcuminoid plus piperine, or placebo) daily, from 7 days before until 3 days after menstruation for three consecutive menstrual cycles. Serum IgE, IL-10 and IL-12 levels were quantified by using an ELISA kit. No significant differences were found between the two groups at baseline, including: age, BMI, and dietary intakes ( P > 0.05). Curcumin + piperine treatment was associated with a significant reduction in the mean serum levels of IgE ; but there were no significant changes in the placebo group ( P = 0.12). Serum concentrations of IL-10 and IL-12 before and after the trial period did not differ significantly between the two groups ( P > 0.05). Curcumin plus piperine might be have positive effect on serum IgE levels with no significant changes on serum IL-10 and IL-12 in healthy young women with PMS and PD. Studies with higher doses and longer durations of treatment with curcumin are required to confirm these findings. In light of increasing research evidence on the molecular mechanisms of allergic diseases, the crucial roles of innate and acquired immunity in the disease’s pathogenesis have been well highlighted. In this respect, much attention has been paid to the modulation of unregulated and unabated inflammatory responses aiming to suppress pathologic immune responses in treating allergic diseases. One of the most important natural compounds with a high potency of immune modulation is curcumin, an active polyphenol compound derived from turmeric, Curcuma longa L, Curcumin’s immunomodulatory action mainly arises from its interactions with an extensive collection of immune cells such as mast cells, eosinophils, epithelial cells, basophils, neutrophils, and lymphocytes. Up to now, there has been no detailed investigation of curcumin’s immunomodulatory actions in allergic diseases. So, the present review study aims to prepare an overview of the immunomodulatory effects of curcumin on the pathologic innate immune responses and dysregulated functions of T helper (T H ) subtypes, including T H 1, T H 2, T H 17, and regulator T cells (Tregs) by gathering evidence from several studies of In-vitro and In-vivo, As the second aim of the present review, we also discuss some novel strategies to overcome the limitation of curcumin in clinical use. Finally, this review also assesses the therapeutic potential of curcumin regarding its immunomodulatory actions in allergic diseases. Curcumin (CUR), demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC) are the main components of turmeric that commonly used to treat neuropathic pain (NP). However, the mechanism of the therapy is not sufficiently clarified. Herein, network pharmacology, molecular docking and molecular dynamics (MD) approaches were used to investigate the mechanism of curcuminoids for NP treatment. Active targets of curcuminoids were obtained from the Swiss Target database, and NP-related targets were retrieved from GeneCards, OMIM, Drugbank and TTD databases. A protein-protein interaction (PPI) network was built to screen the core targets. Furthermore, DAVID was used for GO and KEGG pathway enrichment analyses. Interactions between potential targets and curcuminoids were assessed by molecular docking and the MD simulations were run for 100ns to validate the docking results on the top six complexes. CUR, DMC, and BDMC had 100, 99 and 100 targets respectively. After overlapping with NP there were 33, 33 and 31 targets respectively. PPI network analysis of TOP 10 core targets, TNF, GSK3β were common targets of curcuminoids. Molecular docking and MD results indicated that curcuminoids bind strongly with the core targets. The GO and KEGG showed that curcuminoids regulated nitrogen metabolism, the serotonergic synapse and ErbB signaling pathway to alleviate NP. Furthermore, specific targets in these three compounds were also analysed at the same time. This study systematically explored and compared the anti-NP mechanism of curcuminoids, providing a novel perspective for their utilization. Cow milk allergy is one of the most prevalent food allergies worldwide, particularly in infants and children. To the best of our knowledge, minimal research exists concerning the antigenicity of cow milk (CM). This study was performed to evaluate the allergenicity of enzymatically hydrolyzed cow milk (HM) in a BALB/c mouse model. The mice were randomly divided into 5 groups (n = 12/group), which were sensitized with phosphate-buffered saline, CM, and HM (Alcalase-, or Protamex-, or Flavorzyme-treated cow milk; Novo Nordisk; AT, PT, FT, respectively), respectively, using cholera toxin as adjuvant on d 0, 7, 14, 21. On d 28, the test mice were orally challenged with phosphate-buffered saline, CM, and HM (AT, PT, or FT) alone. Anaphylactic symptoms were monitored in the mice. Antibody, cytokine, histamine, and mouse mast cell protease-1 (mMCP-1) levels were measured using enzyme-linked immunosorbent assays. In addition, the numbers of T helper (Th)1 and Th2 cells, as well as the proportions of CD4 + CD25 + Foxp3 + Treg cells, in mouse spleens were detected using flow cytometry. Statistical significance was determined by one-way ANOVA. The results revealed significant differences between CM- and HM-challenged mice. Among these, the clinical scores of HM-challenged mice (AT, 1.50; PT, 2.00; FT, 1.92) were lower than those of CM-challenged mice (positive control, 2.83), but body weight and temperature of HM-challenged mice were higher than those of CM-challenged mice. In addition, significant reductions of allergen-specific IgE, IgG, histamine, and mMCP-1 were showed in HM-challenged mice, especially for histamine, ranging from 171.42 ng/mL to 214.94 ng/mL. Remarkable reductions of IL-4, IL-5, and IL-13 levels, as well as elevations of interferon-γ and IL-10 levels in the spleens of HM-challenged mice were also detected. Moreover, the number of Th2 cells decreased in the HM-challenged mice, to 2.36% (AT), 1.79% (PT), and 4.03% (FT), respectively, whereas the numbers of Th1 cells (AT, 6.30%; PT, 6.70%; FT, 6.56%) and the proportions of CD4 + CD25 + Foxp3 + Tregs (AT, 8.86%; PT, 9.21%; FT, 9.16%) increased significantly. Our findings indicate that exposure to HM was sufficient to induce a shift toward a Th1 response, thereby reducing potential allergenicity. Importantly, these results will lay a theoretical foundation for the development of hypoallergenic CM products. Cross-cultural comparison of plants used during lactation and the postpartum period offers insight into a largely overlooked area of ethnopharmacological research. Potential roles of phytochemicals in emerging models of interaction among immunity, inflammation, microbiome and nervous system effects on perinatal development have relevance for the life-long health of individuals and of populations in both traditional and contemporary contexts. Delineate and interpret patterns of traditional and contemporary global use of medicinal plants ingested by mothers during the postpartum period relative to phytochemical activity on immune development and gastrointestinal microbiome of breastfed infants, and on maternal health. Published reviews and surveys on galactagogues and postpartum recovery practices plus ethnobotanical studies from around the world were used to identify and rank plants, and ascertain regional use patterns. Scientific literature for 20 most-cited plants based on frequency of publication was assessed for antimicrobial, antioxidant, anti-inflammatory, immunomodulatory, antidepressant, analgesic, galactagogic and safety properties. From compilation of 4418 use reports related to 1948 species, 105 plant taxa were recorded ≥7 times, with the most frequently cited species, Foeniculum vulgare, Trigonella foenum-graecum, Pimpinella anisum, Euphorbia hirta and Asparagus racemosus, 81, 64, 42, 40 and 38 times, respectively. Species and use vary globally, illustrated by the pattern of aromatic plants of culinary importance versus latex-producing plants utilized in North Africa/Middle East and Sub-Saharan Africa with opposing predominance. For 18/20 of the plants a risk/benefit perspective supports assessment that positive immunomodulation and related potential exceed any safety concerns. Published evidence does not support a lactation-enhancing effect for nearly all the most-cited plants while antidepressant data for the majority of plants are predominately limited to animal studies. Within a biocultural context traditional postpartum plant use serves adaptive functions for the mother-infant dyad and contributes phytochemicals absent in most contemporary diets and patterns of ingestion, with potential impacts on allergic, inflammatory and other conditions. Polyphenolics and other phytochemicals are widely immunologically active, present in breast milk and predominately non-toxic. Systematic analysis of phytochemicals in human milk, infant lumen and plasma, and immunomodulatory studies that differentiate maternal ingestion during lactation from pregnancy, are needed. Potential herb-drug interaction and other adverse effects should remain central to obstetric advising, but unless a plant is specifically shown as harmful, considering potential contributions to health of individuals and populations, blanket advisories against postpartum herbal use during lactation appear empirically unwarranted,

Food allergy is an adverse immune response to dietary proteins. Hydrolysates are frequently used for children with milk allergy. However, hydrolysates effects afterwards are poorly studied. The aim of this study was to investigate the immunological consequences of hydrolyzed whey protein in allergic mice. For that, we developed a novel model of food allergy in BALB/c mice sensitized with alum-adsorbed β-lactoglobulin. These mice were orally challenged with either whey protein or whey hydrolysate. Whey-challenged mice had elevated levels of specific IgE and lost weight. They also presented gut inflammation, enhanced levels of SIgA and IL-5 as well as decreased production of IL-4 and IL-10 in the intestinal mucosa. Conversely, mice challenged with hydrolyzate maintained normal levels of IgE, IL-4 and IL-5 and showed no sign of gut inflammation probably due to increased IL-12 production in the gut. Thus, consumption of hydrolysate prevented the development of clinical signs of food allergy in mice. Curcumin has commonly been used for the treatment of various allergic diseases. However, its precise anti-allergic rhinitis effect and mechanism remain unknown. In the present study, the effect of curcumin on allergic responses in ovalbumin (OVA)-induced allergic rhinitis mouse was investigated. We explored the effect of curcumin on the release of allergic inflammatory mediators, such as histamine, OVA-specific IgE, and inflammatory cytokines. Also, we found that curcumin improved rhinitis symptoms, inhibited the histopathological changes of nasal mucosa, and decreased the serum levels of histamine, OVA-specific IgE and TNF-α in OVA-induced allergic rhinitis mice. In addition, curcumin suppressed the production of inflammatory cytokines, such as TNF-α, IL-1β, IL-6 and IL-8. Moreover, curcumin significantly inhibited PMA-induced p-ERK, p-p38, p-JNK, p-Iκ-Bα and NF-κB. These findings suggest that curcumin has an anti-allergic effect through modulating mast cell-mediated allergic responses in allergic rhinitis, at least partly by inhibiting MAPK/NF-κB pathway. Curcumin, phytochemical present in turmeric, rhizome of Curcuma longa, a known anti-inflammatory molecule with variety of pharmacological activities is found effective in murine model of chronic asthma characterized by structural alterations and airway remodeling. Here, we have investigated the effects of intranasal curcumin in chronic asthma where animals were exposed to allergen for longer time. In the present study Balb/c mice were sensitized by an intraperitoneal injection of ovalbumin (OVA) and subsequently challenged with 2% OVA in aerosol twice a week for five consecutive weeks. Intranasal curcumin (5 mg/kg) was administered from days 21 to 55, an hour before every nebulization and inflammatory cells recruitment, levels of IgE, EPO, IL-4 and IL-5 were found suppressed in bronchoalveolar lavage fluid (BALF). Intranasal curcumin administration prevented accumulation of inflammatory cells to the airways, structural alterations and remodeling associated with chronic asthma like peribronchial and airway smooth muscle thickening, sloughing off of the epithelial lining and mucus secretion in ovalbumin induced murine model of chronic asthma. Food allergy is a severe human disease with imminent risk of life. Cissampelos sympodialis (Menispermaceae) is a native Brazilian plant used in Brazilian folk medicine for the treatment of respiratory allergies. In this study the experimental model of food allergy induced by ovalbumin (OVA) was used to determine whether the alcoholic extract of the plant (AFL) and its alkaloids match a therapeutic approach for this disease. Animal weight, diarrhea, OVA-specific IgE levels, inflammatory cell and cytokine profiles, mucus production and proportion of T cells on the mesenteric lymph node (MLN) were evaluated. Warifteine (W) or methyl-warifteine (MW) alkaloids slightly improve diarrhea score independently of AFL and all treatments decreased the OVA-specific IgE levels. Stimulated mesenteric lymph node (MLN) cells in the presence of the alkaloids diminished the IL-12p70 levels independently of IFN-γ or IL-13 secretion. The alkaloids increased the number of Treg cells on MLN and reduced the number of eosinophils and mast cells as well as mucus production in the gut. Therefore, the alkaloids modulate the immune response in food allergy by increasing regulatory T cells in MLN independently of Th1 or Th2 profiles. In our mouse model, gastric acid-suppression is associated with antigen-specific IgE and anaphylaxis development. We repeatedly observed non-responder animals protected from food allergy. Here, we aimed to analyse reasons for this protection. Ten out of 64 mice, subjected to oral ovalbumin (OVA) immunizations under gastric acid-suppression, were non-responders without OVA-specific IgE or IgG1 elevation, indicating protection from allergy. In these non-responders, allergen challenges confirmed reduced antigen uptake and lack of anaphylactic symptoms, while in allergic mice high levels of mouse mast-cell protease-1 and a body temperature reduction, indicative for anaphylaxis, were determined. Upon OVA stimulation, significantly lower IL-4, IL-5, IL-10 and IL-13 levels were detected in non-responders, while IL-22 was significantly higher. Comparison of fecal microbiota revealed differences of bacterial communities on single bacterial Operational-Taxonomic-Unit level between the groups, indicating protection from food allergy being associated with a distinct microbiota composition in a non-responding phenotype in this mouse model. Alginate is a dietary polysaccharide that exerts antioxidative, immunomodulatory and anti-allergic effects. In this study, the effects of alginate on the secondary structure of ovalbumin (OVA) in vitro and on the regulation of OVA-induced gut microbiota disorders in vivo were investigated. First, the interactions between OVA and alginate were studied by multiple spectroscopic methods, which showed that alginate could change the secondary structure of OVA. Then, the regulation of allergic diarrhoea by alginate was evaluated in OVA-sensitized mice, which demonstrated that alginate could attenuate allergic diarrhoea and duodenal morphological damage. Additionally, when diarrhoea symptoms were ameliorated by alginate, the richness and diversity of the gut microbiota could be partially restored, and the relative abundances of Alloprevotella, Bacteroides, Parabacteroides and Rikenellaceae_RC9_gut_group showed recovery trends. Therefore, alginate could improve OVA-induced gut microbiota disorder, and alginate could be used as a potential agent for intestinal protection in the food or pharmaceutical industry.

: Turmeric (Curcuma longa) attenuates food allergy symptoms by regulating type 1/type 2 helper T cells (Th1/Th2) balance in a mouse model of food allergy

What foods cause high IgE levels?

IgE-mediated food allergies cause your child’s immune system to react abnormally when exposed to one or more specific foods such as milk, egg, wheat or nuts. Children with this type of food allergy will react quickly — within a few minutes to a few hours.

Milk Egg Soy Wheat Peanut Tree nuts Fish Shellfish

All of these foods can trigger anaphylaxis (a severe, whole-body allergic reaction) in patients who are allergic. Food allergies are common: 5 percent of children under the age of five have a food allergy and roughly 4 percent of adolescents and adults have a food allergy.

The prevalence of food allergies does seem to be increasing. Researchers at The Children’s Hospital of Philadelphia are evaluating the genetics of food allergy and possible reasons for the increase in all allergic conditions. Researchers believe many factors may play a role in food allergy development including maternal diet during pregnancy, timing of food introduction, and breastfeeding status.

How to fight allergies naturally, histamine and antihistamine food

If you have an “allergic family” — one that includes family members with asthma, environmental allergies and eczema — your child has an increased risk for allergy. When IgE is working properly, it identifies triggers — such as parasites or other items that could be harmful to the body — and tells the body to release histamine.

• Histamine causes symptoms such as cough, wheeze and hives.
• However, IgE can sometimes react to normal proteins, causing your child’s body to react to a specific food protein or proteins.
• Once a food is eaten, the protein is absorbed during digestion and enters the bloodstream.
• That food will cause symptoms throughout the body because of IgE.

For example, if your child has an IgE-mediated allergy to the protein in milk, he may experience symptoms in the skin (hives), stomach (vomiting), lungs (coughing, wheezing), and circulatory system (decreasing blood pressure). When your child has a food allergy, her body’s IgE antibodies identify that specific food as an invader and can produce symptoms in multiple areas of the body, including:

Skin: “hives” (red blotches or welts that itch), mild to severe swelling Eyes: tearing, redness, itch Nose: clear discharge, itch, congestion Mouth: itch, lip swelling, tongue swelling Throat: tightness, trouble speaking, trouble inhaling Lungs: shortness of breath, rapid breathing, cough, wheeze Stomach: repeated vomiting, nausea, abdominal pain, diarrhea (usually later) Heart and circulation: weak pulse, loss of consciousness Brain: anxiety, agitation, loss of consciousness

Allergic reactions can be scary, but noticing symptoms early can help your child get proper treatment. Reactions to food can be different every time. Your child’s reaction can depend on a variety of factors including the amount of food eaten, uncontrolled asthma, and illness.

Your child may have had a reaction to a food which led to an evaluation by an allergist Your child may have had a flare of eczema, which led to concerns about a food allergy You may have discussed concerns about your child with her pediatrician, who recommended consultation with a specialist

When you meet with allergy specialists at The Children’s Hospital of Philadelphia, we will discuss your child’s food reaction history, as well as get a detailed medical and family history. Based on your child’s history and findings, our allergy specialists may recommend testing.