Difference Between Infection And Inflammation

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Difference Between Infection And Inflammation
Inflammation is not a synonym for infection, even in cases where inflammation is caused by infection. Although infection is caused by a microorganism, inflammation is one of the responses of the organism to the pathogen.

Can you have inflammation without infection?

Measuring inflammation – When inflammation is present in the body, there will be higher levels of substances known as biomarkers. An example of a biomarker is C-reactive protein (CRP), If a doctor wants to test for inflammation, they may assess CRP levels.

Is inflammation a response to infection?

INTRODUCTION – Inflammation is the immune system’s response to harmful stimuli, such as pathogens, damaged cells, toxic compounds, or irradiation, and acts by removing injurious stimuli and initiating the healing process, Inflammation is therefore a defense mechanism that is vital to health,

Usually, during acute inflammatory responses, cellular and molecular events and interactions efficiently minimize impending injury or infection. This mitigation process contributes to restoration of tissue homeostasis and resolution of the acute inflammation. However, uncontrolled acute inflammation may become chronic, contributing to a variety of chronic inflammatory diseases,

At the tissue level, inflammation is characterized by redness, swelling, heat, pain, and loss of tissue function, which result from local immune, vascular and inflammatory cell responses to infection or injury, Important microcirculatory events that occur during the inflammatory process include vascular permeability changes, leukocyte recruitment and accumulation, and inflammatory mediator release,

  • Various pathogenic factors, such as infection, tissue injury, or cardiac infarction, can induce inflammation by causing tissue damage.
  • The etiologies of inflammation can be infectious or non-infectious (Table ​ 1 ).
  • In response to tissue injury, the body initiates a chemical signaling cascade that stimulates responses aimed at healing affected tissues.

These signals activate leukocyte chemotaxis from the general circulation to sites of damage. These activated leukocytes produce cytokines that induce inflammatory responses,

Can a bacterial infection cause inflammation?

What is inflammation? – When your body encounters an offending agent (like viruses, bacteria or toxic chemicals) or suffers an injury, it activates your immune system, Your immune system sends out its first responders: inflammatory cells and cytokines (substances that stimulate more inflammatory cells).

What comes first inflammation or infection?

Correspondence – Dear Editor, The review recently published by Autio et al. entitled ‘Nuclear imaging of inflammation: homing-associated molecules as targets’ contains some statement that may be misleading and requires some clarification. In particular, I think it is important to correctly define the terms ‘inflammation’ and ‘infection.’ Just by reading the definition of inflammation in the Wikipedia, we learn that ‘inflammation is part of the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.

  1. The classical signs of acute inflammation are pain ( dolor ), heat ( calor ), redness ( rubor ), swelling ( tumor ), and loss of function ( functio laesa ).
  2. Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process.
  3. Inflammation is not a synonym for infection, even in cases where inflammation is caused by infection.

Although infection is caused by a microorganism, inflammation is one of the responses of the organism to the pathogen. However, inflammation is a stereotyped response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen’,

Similarly, we can find a definition for infection as ‘the invasion of a host organism’s bodily tissues by disease-causing organisms, their multiplication, and the reaction of host tissues to these organisms and the toxins they produce. Infections are caused by microorganisms such as viruses, prions, bacteria, and viroids, and larger organisms like parasites and fungi.

Hosts can fight infections using their immune system. Mammalian hosts react to infections with an innate response, often involving inflammation, followed by an adaptive response’. Therefore, we usually always have an inflammation associated with an infection, but not always we have an infection if there is an inflammation,

This is not just an exercise of semantics, but it is very relevant, particularly for the nuclear medicine point of view. Indeed, nuclear medicine techniques aim at differentiating ‘sterile inflammation’ from infection and the two terms cannot be used as synonyms. It emerges, as a consequence of what we defined above, that a good radiopharmaceutical for imaging infection should not image inflammation.

This is not always easy, and a certain amount of radiopharmaceutical accumulation in sites of sterile inflammation can often be noticed when seeking for infection. In case of radiolabeled white blood cells (WBC) and radiolabeled anti-granulocyte monoclonal antibodies, the specificity for infection can be improved by optimizing the image acquisition and interpretation protocols.

  • These protocols are currently being standardized by the EANM Committee on infection/inflammation imaging, but most users of WBC already know and successfully apply these criteria.
  • In short, images should be acquired at three time points (30 min to 1 h, also called ‘early image’; 3 to 4 h, also called ‘delayed image’; and 20 to 24 h post-injection, also called ‘late image’) in a time-corrected manner for isotope decay.

Then, images are displayed with the same intensity scale, and any focal increase of activity or size with time should be considered an infection, whereas an accumulation at 3 to 4 h with a decrease at 20 to 24 h is a sign of a sterile inflammation. As mentioned, it is important that in papers and reviews, we learn to use the correct terminology in order not to create confusion to the readers.

The sentence reported in the Abstract by Autio et al. ‘the golden standard in nuclear medicine imaging of inflammation is the use of autologous radiolabeled leukocytes’ is therefore misleading, being WBC the gold standard technique for imaging infection. Furthermore, in the Introduction, it is reported that ‘non-invasive imaging of inflammation could be a highly valuable tool as it could help diagnosing many inflammatory conditions, such as osteomyelitis, rheumatoid arthritis, sarcoidosis, inflammatory bowel disease, and fever of unknown origin.’ These diseases cannot be pooled together.

We should clarify that the aim of nuclear medicine in osteomyelitis is to image infection. In sarcoidosis and rheumatoid arthritis, we aim at imaging inflammation, and therefore, many ‘granulocyte-based approaches’ are useless and FDG and anti-TNFa MoAb seem much better agents by targeting monocytes and other inflammatory cells/components,

In IBD and FUO, the situation is much more complicated as we might need to image either the inflammatory events or the sites of pathological granulocyte accumulation (abscesses, fistulae, inflammatory stenosis, etc.). In all cases, it is extremely important to keep a distinction between inflammation and infection, to use the appropriate terminology, and to keep in mind that we have radiopharmaceuticals designed specifically for infection imaging and others that are more appropriate for sterile inflammation imaging (such as sarcoidosis, vasculitis, rheumatoid arthritis, atherosclerosis, autoimmune diseases, degenerative diseases, etc.).

This is not clearly emerging from the review of Autio et al. and may lead to some confusion.

Are the signs of infection and inflammation the same?

You may hear the words infection and inflammation together, but they mean very different things. Infection refers to the invasion and multiplication of bacteria or viruses within the body, while inflammation is the body’s protective response against infection.

What are the 5 classic signs of inflammation?

Introduction – Based on visual observation, the ancients characterised inflammation by five cardinal signs, namely redness ( rubor ), swelling ( tumour ), heat ( calor ; only applicable to the body’ extremities), pain ( dolor ) and loss of function ( functio laesa ).

  1. The first four of these signs were named by Celsus in ancient Rome (30–38 B.C.) and the last by Galen (A.D 130–200),
  2. More recently, inflammation was described as “the succession of changes which occurs in a living tissue when it is injured provided that the injury is not of such a degree as to at once destroy its structure and vitality”, or “the reaction to injury of the living microcirculation and related tissues,

Although, in ancient times inflammation was recognised as being part of the healing process, up to the end of the 19 th century, inflammation was viewed as being an undesirable response that was harmful to the host. However, beginning with the work of Metchnikoff and others in the 19 th century, the contribution of inflammation to the body’s defensive and healing process was recognised,

Furthermore, inflammation is considered the cornerstone of pathology in that the changes observed are indicative of injury and disease. The classical description of inflammation accounts for the visual changes seen. Thus, the sensation of heat is caused by the increased movement of blood through dilated vessels into the environmentally cooled extremities, also resulting on the increased redness (due to the additional number of erythrocytes passing through the area).

The swelling (oedema) is the result of increased passage of fluid from dilated and permeable blood vessels into the surrounding tissues, infiltration of cells into the damaged area, and in prolonged inflammatory responses deposition of connective tissue.

Pain is due to the direct effects of mediators, either from initial damage or that resulting from the inflammatory response itself, and the stretching of sensory nerves due to oedema. The loss of function refers to either simple loss of mobility in a joint, due to the oedema and pain, or to the replacement of functional cells with scar tissue.

Today it is recognised that inflammation is far more complex than might first appear from the simple description given above and is a major response of the immune system to tissue damage and infection, although not all infection gives rise to inflammation.

  1. Inflammation is also diverse, ranging from the acute inflammation associated with S.
  2. Aureus infection of the skin (the humble boil), through to chronic inflammatory processes resulting in remodeling of the artery wall in atherosclerosis; the bronchial wall in asthma and chronic bronchitis, and the debilitating destruction of the joints associated with rheumatoid arthritis.
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These processes involve the major cells of the immune system, including neutrophils, basophils, mast cells, T-cells, B-cells, etc. However, examination of a range of inflammatory lesions demonstrates the presence of specific leukocytes in any given lesion.

That is, the inflammatory process is regulated in such a way as to ensure the appropriate leukocytes are recruited. These events are controlled by a host of extracellular mediators and regulators, including cytokines, growth factors, eicosanoids (prostaglandins, leukotrines, etc), complement and peptides.

In fact, it is the discovery of many of these mediators over the past 20 years that has increased our understanding of the regulation of the inflammatory process whilst, at the same time, revealing its complexity. These extracellular events are matched by equally complex intracellular signalling control mechanisms, with the ability of cells to assemble and disassemble an almost bewildering array of signalling pathways as they move from inactive to dedicated roles within the inflammatory response and site.

Which cells and mediators come into play depends on wide range of factors. These include: what stage the process of inflation is at; the initiating event, i.e. type of pathogen, auto-immune, chemical or physical injury, etc.; the tissue or organ involved; whether the inflammation is of an acute, resolving form or chronic, non resolving or long-lasting type; whether formation of granuloma is involved, or whether scarring results.

The role of inflammation as a healing, restorative process, as well as its aggressive role, is also more widely recognised today. Inflammation is now considered as the full circle of events, from initiation of a response, through the development of the cardinal signs above, to healing and restoration of normal appearance and function of the tissue or organ.

  1. However, in certain conditions there appears to be no resolution and a chronic state of inflammation develops that may last the life of the individual.
  2. Such conditions include the inflammatory disorders rheumatoid arthritis, osteoarthritis, inflammatory bowel diseases, retinitis, multiple sclerosis, psoriasis and atherosclerosis.

In order to study inflammation a multidisciplinary approach is necessary. Classically, it has required the study of the immune system, in order to understand the events involved in initiating and maintaining inflammatory conditions. Today it is recognised that the underlying genetics and molecular biology basis to cellular responses are also important in order to identify genetic predisposition to inflammatory diseases, while pharmacological studies are necessary to identify targets and develop novel treatments to bring relief from chronic life-threatening inflammatory conditions.

  1. Thus research into inflammation includes not only the study of immunological and cellular responses involved but also the pharmacological process involved in drug development.
  2. Many of the drugs used in the treatment of inflammatory conditions, predate our current understanding of the biochemical processes involved in the disease.

Traditionally, the standard treatments for rheumatoid arthritis has been to use a non-steroidal anti-inflammatory drug (NSAID), such as aspirin, for pain relief and to use corticosteroids or even disease-modifying anti-rheumatic drugs in an attempt to reduce other symptoms of the disease.

For many years the pharmaceutical industry attempted to develop NSAIDs which shared the therapeutic action of aspirin but which did not cause the main adverse event, namely gastric ulceration. This research led to the development of indomethacin, the fenamates, ibuprofen and many others. However, while all these drugs had clinical utility they also eroded the gastric mucosa.

In addition, this research also led to the development of some of the animal models still used in arthritis research today, such as carrageenin oedema and adjuvant arthritis ). The development of NSAIDs, with reduced potential to cause gastric ulcers, was finally realised with the demonstration that clinically useful NSAIDs inhibited the enzyme cyclo-oxygenase, which was also present in the gastric mucosa.

  1. The finding that cyclo-oxygenase present in inflammatory lesions (COX2) was distinct from that found in the stomach (COX1) led to the development of selective COX2 inhibitors, such as celecoxib.
  2. These drugs provide relief from many of the symptoms of arthritis but have a reduced potential to cause gastric ulceration,

The differential responsiveness to these, and other, therapeutic agents and, indeed, the induction of the inflammatory response in some patients with asthma by aspirin, has led to the concept of pharmacogenomics to understand individual drug sensitivities with a view to producing therapy tailored to the individual.

  • Similarly, glucocorticoids are widely used in the treatment of inflammation.
  • Unlike the NSAIDs these agents do not relieve pain but reduce inflammation by inhibiting leukocyte function.
  • The active ingredient responsible for the anti-inflammatory activity of adrenal cortex extracts was discovered in the 1940s.

This led to the use of cortisol as an anti-inflammatory and the development of potent synthetic agents typified by dexamethasone. However, because cortisol, and synthetic glucocorticoids, produce their therapeutic action at supra-physiological concentrations, adverse effects, such as suppression of the HPA-axis and Cushingoid changes are inevitable.

  • Many of these adverse effects can be avoided by giving glucocorticoids topically.
  • This has led to the development of inhaled glucocorticoids for the treatment of inflammatory diseases of the respiratory tract and steroid containing creams for the treatment of skin inflammation.
  • However, applying this approach to the treatment of rheumatoid arthritis necessitates the use of intra-articular injection.

Thus, there is a clear unmet medical need for a drug that provides relief from the symptoms of inflammation but can be given systemically. The fact that a large number of patients with severe chronic inflammatory disease fail to respond to conventional systemic or topical therapy resulting in a huge clinical and socio-economic burdon underlies the need to develop novel therapies.

Thus, modern research has used molecular techniques to identify which genes are regulated by glucocorticoid receptors in an attempt to identify novel therapeutic targets. This work has attempted to fine tune the immune system through use of agents that inhibit specific pathways and mediators rather than to suppress immune cell activity.

Examples of such approaches include the development of anti-TNFa therapies, anti adhesion molecule therapies and inhibitors of cytokines believed to be pivotal in a given pathology, Furthermore, inhibitors of selective pro-inflammatory intracellular signalling pathways are currently in use e.g.

  • Cyclsporin or under development e.g.
  • NF-κB, p38 MAPK and PDE4 inhibitors,
  • As we understand more about the complexity of the inflammatory response and the actions of the currently available drugs the value of particular clusters of targets becomes apparent.
  • However, the success of anti-TNFα therapy in RA underlines the importance of understanding/discovering the initial driver(s) of the inflammatory response in individual diseases and patients.

While research into inflammation has resulted in great progress in the latter half of the 20th century, we recognise that the rate of progress is accelerating. Furthermore, it is our perception that there is a need for a vehicle through which this very diverse research can readily be made available to the scientific community.

Do antibiotics get rid of inflammation?

Why do antibiotics work if it is not a sinus infection? Does this describe you? “Every time I’m on antibiotics I feel better but when I stop them I feel worse again.” And then a bombshell hits: your doctor tells you that YOU DON’T HAVE A SINUS INFECTION! How could this be? Let’s explore this.

You actually have a resistant or refractory sinus infection. Okay, this is straightforward, find the underlying cause and treat. You do not have a bacterial sinus infection, and the reason for recurrence is that antibiotics are not the best treatment. Many scenarios fit in this category, including but not limited to, allergies, viral colds, and headache syndromes.

But let’s get back to the point. If the condition is NOT a bacterial infection, why would antibiotics make you feel better? There are a few reasons for this phenomenon. Many processes that make a person feel miserable are related to inflammatory responses.

  • The Common Cold causes inflammation in the nasopharyngeal tract.
  • Tension headaches are related to inflammation of the head and face muscles.
  • Certain antibiotics have been shown to reduce inflammation because of its anti-inflamatory properties (1).
  • Hence, raises the question, anti-inflammatory vs antibiotics? Reducing inflammation reduces the symptoms, thereby making it appear that the antibiotics are working.

But if the right diagnosis can be made, better treatments than antibiotics can be considered. A placebo effect is a phenomenon when a drug produces a beneficial effect not attributable to the drug’s properties. Sometimes, the human body will produce its own opioid chemicals (called endogenous opioids) in response to the belief that a treatment works, even if that treatment is a salt-water pill! Thus, some of the effect of antibiotics in nonbacterial conditions can be related to placebo (4).

Some antibiotics appear to modulate the pain centers and processes in the body (2,3), which would make a headache less intense and reduce symptoms of a viral Cold even if no bacteria are present! There are better treatments for these conditions than antibiotics though. So what? So what if it is not a bacteria sinus infection.

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If it makes you feel better, why not take antibiotics or antibiotic therapy? This question is great, and you need to know the answer, not just for yourself but for your elderly family member who, as frail as can be, may at any point get a resistant, life-threatening infection.

If that is the case then, do we use nonsteroidal anti-inflamatory drugs or anti-inflammatory treatment instead of antibiotic treatment? Bacteria are keen adapters, and they become resistant to antibiotics to which they are frequently exposed. Increasing resistance to antibiotics has been demonstrated and inappropriate antibiotic use continues to worsen this pattern (5).

Thus, antibiotics should be reserved for bacterial infections. References

Amsden GW. Anti-inflammatory effects of macrolides—an underappreciated benefit in the treatment of community-acquired respiratory tract infections and chronic inflammatory pulmonary conditions? J Antimicrob Chemother.2005 Jan;55(1):10-21. Suaudeau C, de Beaurepaire R, Rampin O, Albe-Fessard D. Antibiotics and morphinomimetic injections prevent automutilation behavior in rats after dorsal rhizotomy. Clin J Pain.1989;5(2):177–181. Ocana M, Baeyens JM. Analgesic effects of centrally administered aminoglycoside antibiotics in mice. Neurosci Lett.1991;126(1):67–70. Amanzio M, Benedetti F. Neuropharmacological dissection of placebo analgesia: expectation-activated opioid systems versus conditioning-activated specific subsystems. J Neurosci.1999 Jan 1;19(1):484–494. Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, Harrison LH, Lynfield R, Dumyati G, Townes JM, Craig AS, Zell ER, Fosheim GE, McDougal LK, Carey RB, Fridkin SK. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA.2007;298(15):1763–1771.

: Why do antibiotics work if it is not a sinus infection?

Can your body fight an infection without antibiotics?

Be Antibiotics Aware: Smart Use, Best Care is the Centers for Disease Control and Prevention’s (CDC) national educational effort to help improve antibiotic prescribing and use and combat antibiotic resistance. is one of the most urgent threats to the public’s health. Antibiotic resistance happens when germs, like bacteria and fungi, develop the ability to defeat the drugs designed to kill them.

  • That means the germs are not killed and continue to grow.
  • More than 2.8 million antibiotic-resistant infections occur in the United States each year, and more than 35,000 people die as a result.
  • Antibiotics can save lives, but any time antibiotics are used, they can cause side effects and contribute to the development of antibiotic resistance.

Each year, at least 28% of antibiotics are prescribed unnecessarily in U.S. doctors’ offices and emergency rooms (ERs), which makes improving antibiotic prescribing and use a national priority. Helping healthcare professionals improve the way they prescribe antibiotics, and improving the way we take antibiotics, helps keep us healthy now, helps fight antibiotic resistance, and ensures that these life-saving drugs will be available for future generations.

Antibiotics are only needed for treating certain infections caused by bacteria, but even some bacterial infections get better without antibiotics. We rely on antibiotics to treat serious, life-threatening conditions such as pneumonia and, the body’s extreme response to an infection. Effective antibiotics are also needed for people who are at high risk for developing infections.

Some of those at high risk for infections include patients undergoing surgery, patients with end-stage kidney disease, or patients receiving cancer therapy (chemotherapy).

Antibiotics DO NOT work on viruses, such as those that cause colds, flu, or,Antibiotics also are not needed for many sinus infections and some ear infections.When antibiotics aren’t needed, they won’t help you, and the side effects could still cause harm. Common side effects of antibiotics can include:

Rash Dizziness Nausea Diarrhea Yeast infections

More serious side effects can include:

infection (also called difficile or C. diff ), which causes severe diarrhea that can lead to severe colon damage and death Severe and life-threatening allergic reactions, such as wheezing, hives, shortness of breath, and anaphylaxis (which also includes feeling like your throat is closing or choking, or your voice is changing)

Antibiotic use can also lead to the development of antibiotic resistance.

A sk your healthcare professional about the best w ay to feel better while your body fights off the virus. If you need antibiotics, take them exactly as prescribed. Talk with your healthcare professional if you have any questions about your antibiotics. Talk with your healthcare professional if you develop any side effects, especially severe diarrhea, since that could be a C. diff. infection, which needs to be treated immediately. Do your best to stay healthy and keep others healthy:

Clean hands by washing with soap and water for at least 20 seconds or use a hand sanitizer that contains at least 60% alcohol Cover your mouth and nose with a tissue when you cough or sneeze Stay home when sick Get recommended vaccines, such as the vaccine.

To learn more about antibiotic prescribing and use, visit, To learn more about antibiotic resistance, visit, : Be Antibiotics Aware: Smart Use, Best Care

How do you know if your body is fighting a bacterial infection?

What are the symptoms of a bacterial infection? – The symptoms of a bacterial infection depend on the location of your infection and the type of bacteria involved. There are some general signs of bacterial infection:

fever feeling tired swollen lymph nodes in your neck, armpits, groin or elsewhere headache nausea or vomiting

CHECK YOUR SYMPTOMS — Use the Symptom Checker and find out if you need to seek medical help.

Does inflammation heal on its own?

How can you tell the difference between acute and chronic inflammation? –

  • There are three distinct differences between acute inflammation that’s a healthy part of your immune response and unhealthy chronic inflammation that is associated with disease: duration, cause and symptoms.
  • Acute inflammation will only last a couple days to weeks, whereas chronic inflammation lasts months to years.
  • Causes of acute inflammation include exposure to bacteria, fungi, a foreign object or environmental toxins, whereas chronic inflammation is caused by consistent exposure to toxins or pollution, autoimmune disorders,genetic factors, or an inability to return to baseline after an acute inflammation.
  • As for symptoms, there are some telling differences.
  • “Classic signs of acute inflammation include redness, swelling and the spot being warm to the touch,” Lang says.

Acute inflammation tends to be a bit painful, causing a throbbing or pinching sensation at the site of inflammation. In cases like the common cold, you might also have a fever, muscle stiffness, or aches and pains. And if you’ve ever dealt with an or sore throat, you’ve experienced acute inflammation in all its red, swollen glory.

Symptoms of chronic inflammation tend to be less noticeable, harder to identify and may vary based on associated conditions. For example, if you have, you might experience chronic inflammation in your joints; while if you have asthma, you may develop scarring or fibrosis due to inflammation, Lang says.

Other symptoms of chronic inflammation include abdominal or chest pain, fever and fatigue. Long story short? If you’re experiencing short-term redness, sensitivity or swelling due to a cold or cut, you’re dealing with acute inflammation, which should heal soon on its own.

How does inflammation feel like?

Some of the most common signs of chronic inflammation include: Body discomfort, including joint stiffness, tendonitis and muscle pain. Sleep disorders like insomnia, sleep apnea and persistent fatigue.

Can you tell if your body is fighting an infection?

Signs and symptoms of an infection – You could have one or more of the following symptoms:

a change in your temperature – 37.5°C or higher or below 36°Cfeeling generally unwell – not able to get out of bedflu-like symptoms – feeling cold and shivery, headaches, and aching musclescoughing up green phlegm a sore throat or sore moutha throbbing, painful toothpain having a wee, going more often or cloudy or foul-smelling wee diarrhoea – 4 or more loose, watery bowel movements in 24 hoursskin changes – redness, feeling hot, swelling or paina fast heartbeatquick breathing or feeling short of breathfeeling dizzy or faint feeling confused or disorientated being sick (vomiting) a headachepain, redness, discharge, swelling or heat at the site of a wound or intravenous line such as a central line or PICC line pain anywhere in your body that was not there before your treatment

An increase in your temperature to 37.5C or higher might be the first sign that you have an infection. Call your 24 hour advice line immediately, you might need injections of antibiotics to control the infection.

Does swelling always mean infection?

6. Swelling of Wounded Area – Like redness, swelling is normal at the beginning stages of wound healing. However, swelling should be continually decreasing. Persistent swelling could be a further sign of infection or other complications.

Can inflammation be normal?

Inflammation is a normal part of the body’s defense to injury or infection, and, in this way, it is beneficial. But inflammation is damaging when it occurs in healthy tissues or lasts too long. Known as chronic inflammation, it may persist for months or years.

What are the 5 classic signs of inflammation?

Introduction – Based on visual observation, the ancients characterised inflammation by five cardinal signs, namely redness ( rubor ), swelling ( tumour ), heat ( calor ; only applicable to the body’ extremities), pain ( dolor ) and loss of function ( functio laesa ).

The first four of these signs were named by Celsus in ancient Rome (30–38 B.C.) and the last by Galen (A.D 130–200), More recently, inflammation was described as “the succession of changes which occurs in a living tissue when it is injured provided that the injury is not of such a degree as to at once destroy its structure and vitality”, or “the reaction to injury of the living microcirculation and related tissues,

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Although, in ancient times inflammation was recognised as being part of the healing process, up to the end of the 19 th century, inflammation was viewed as being an undesirable response that was harmful to the host. However, beginning with the work of Metchnikoff and others in the 19 th century, the contribution of inflammation to the body’s defensive and healing process was recognised,

Furthermore, inflammation is considered the cornerstone of pathology in that the changes observed are indicative of injury and disease. The classical description of inflammation accounts for the visual changes seen. Thus, the sensation of heat is caused by the increased movement of blood through dilated vessels into the environmentally cooled extremities, also resulting on the increased redness (due to the additional number of erythrocytes passing through the area).

The swelling (oedema) is the result of increased passage of fluid from dilated and permeable blood vessels into the surrounding tissues, infiltration of cells into the damaged area, and in prolonged inflammatory responses deposition of connective tissue.

Pain is due to the direct effects of mediators, either from initial damage or that resulting from the inflammatory response itself, and the stretching of sensory nerves due to oedema. The loss of function refers to either simple loss of mobility in a joint, due to the oedema and pain, or to the replacement of functional cells with scar tissue.

Today it is recognised that inflammation is far more complex than might first appear from the simple description given above and is a major response of the immune system to tissue damage and infection, although not all infection gives rise to inflammation.

Inflammation is also diverse, ranging from the acute inflammation associated with S. aureus infection of the skin (the humble boil), through to chronic inflammatory processes resulting in remodeling of the artery wall in atherosclerosis; the bronchial wall in asthma and chronic bronchitis, and the debilitating destruction of the joints associated with rheumatoid arthritis.

These processes involve the major cells of the immune system, including neutrophils, basophils, mast cells, T-cells, B-cells, etc. However, examination of a range of inflammatory lesions demonstrates the presence of specific leukocytes in any given lesion.

  1. That is, the inflammatory process is regulated in such a way as to ensure the appropriate leukocytes are recruited.
  2. These events are controlled by a host of extracellular mediators and regulators, including cytokines, growth factors, eicosanoids (prostaglandins, leukotrines, etc), complement and peptides.

In fact, it is the discovery of many of these mediators over the past 20 years that has increased our understanding of the regulation of the inflammatory process whilst, at the same time, revealing its complexity. These extracellular events are matched by equally complex intracellular signalling control mechanisms, with the ability of cells to assemble and disassemble an almost bewildering array of signalling pathways as they move from inactive to dedicated roles within the inflammatory response and site.

Which cells and mediators come into play depends on wide range of factors. These include: what stage the process of inflation is at; the initiating event, i.e. type of pathogen, auto-immune, chemical or physical injury, etc.; the tissue or organ involved; whether the inflammation is of an acute, resolving form or chronic, non resolving or long-lasting type; whether formation of granuloma is involved, or whether scarring results.

The role of inflammation as a healing, restorative process, as well as its aggressive role, is also more widely recognised today. Inflammation is now considered as the full circle of events, from initiation of a response, through the development of the cardinal signs above, to healing and restoration of normal appearance and function of the tissue or organ.

  1. However, in certain conditions there appears to be no resolution and a chronic state of inflammation develops that may last the life of the individual.
  2. Such conditions include the inflammatory disorders rheumatoid arthritis, osteoarthritis, inflammatory bowel diseases, retinitis, multiple sclerosis, psoriasis and atherosclerosis.

In order to study inflammation a multidisciplinary approach is necessary. Classically, it has required the study of the immune system, in order to understand the events involved in initiating and maintaining inflammatory conditions. Today it is recognised that the underlying genetics and molecular biology basis to cellular responses are also important in order to identify genetic predisposition to inflammatory diseases, while pharmacological studies are necessary to identify targets and develop novel treatments to bring relief from chronic life-threatening inflammatory conditions.

Thus research into inflammation includes not only the study of immunological and cellular responses involved but also the pharmacological process involved in drug development. Many of the drugs used in the treatment of inflammatory conditions, predate our current understanding of the biochemical processes involved in the disease.

Traditionally, the standard treatments for rheumatoid arthritis has been to use a non-steroidal anti-inflammatory drug (NSAID), such as aspirin, for pain relief and to use corticosteroids or even disease-modifying anti-rheumatic drugs in an attempt to reduce other symptoms of the disease.

For many years the pharmaceutical industry attempted to develop NSAIDs which shared the therapeutic action of aspirin but which did not cause the main adverse event, namely gastric ulceration. This research led to the development of indomethacin, the fenamates, ibuprofen and many others. However, while all these drugs had clinical utility they also eroded the gastric mucosa.

In addition, this research also led to the development of some of the animal models still used in arthritis research today, such as carrageenin oedema and adjuvant arthritis ). The development of NSAIDs, with reduced potential to cause gastric ulcers, was finally realised with the demonstration that clinically useful NSAIDs inhibited the enzyme cyclo-oxygenase, which was also present in the gastric mucosa.

The finding that cyclo-oxygenase present in inflammatory lesions (COX2) was distinct from that found in the stomach (COX1) led to the development of selective COX2 inhibitors, such as celecoxib. These drugs provide relief from many of the symptoms of arthritis but have a reduced potential to cause gastric ulceration,

The differential responsiveness to these, and other, therapeutic agents and, indeed, the induction of the inflammatory response in some patients with asthma by aspirin, has led to the concept of pharmacogenomics to understand individual drug sensitivities with a view to producing therapy tailored to the individual.

  1. Similarly, glucocorticoids are widely used in the treatment of inflammation.
  2. Unlike the NSAIDs these agents do not relieve pain but reduce inflammation by inhibiting leukocyte function.
  3. The active ingredient responsible for the anti-inflammatory activity of adrenal cortex extracts was discovered in the 1940s.

This led to the use of cortisol as an anti-inflammatory and the development of potent synthetic agents typified by dexamethasone. However, because cortisol, and synthetic glucocorticoids, produce their therapeutic action at supra-physiological concentrations, adverse effects, such as suppression of the HPA-axis and Cushingoid changes are inevitable.

Many of these adverse effects can be avoided by giving glucocorticoids topically. This has led to the development of inhaled glucocorticoids for the treatment of inflammatory diseases of the respiratory tract and steroid containing creams for the treatment of skin inflammation. However, applying this approach to the treatment of rheumatoid arthritis necessitates the use of intra-articular injection.

Thus, there is a clear unmet medical need for a drug that provides relief from the symptoms of inflammation but can be given systemically. The fact that a large number of patients with severe chronic inflammatory disease fail to respond to conventional systemic or topical therapy resulting in a huge clinical and socio-economic burdon underlies the need to develop novel therapies.

Thus, modern research has used molecular techniques to identify which genes are regulated by glucocorticoid receptors in an attempt to identify novel therapeutic targets. This work has attempted to fine tune the immune system through use of agents that inhibit specific pathways and mediators rather than to suppress immune cell activity.

Examples of such approaches include the development of anti-TNFa therapies, anti adhesion molecule therapies and inhibitors of cytokines believed to be pivotal in a given pathology, Furthermore, inhibitors of selective pro-inflammatory intracellular signalling pathways are currently in use e.g.

cyclsporin or under development e.g. NF-κB, p38 MAPK and PDE4 inhibitors, As we understand more about the complexity of the inflammatory response and the actions of the currently available drugs the value of particular clusters of targets becomes apparent. However, the success of anti-TNFα therapy in RA underlines the importance of understanding/discovering the initial driver(s) of the inflammatory response in individual diseases and patients.

While research into inflammation has resulted in great progress in the latter half of the 20th century, we recognise that the rate of progress is accelerating. Furthermore, it is our perception that there is a need for a vehicle through which this very diverse research can readily be made available to the scientific community.

Does inflammation always show up in blood tests?

Are tests for inflammation useful? – In certain situations, tests to measure inflammation can be quite helpful.

Diagnosing an inflammatory condition. One example of this is a rare condition called, in which the ESR is nearly always elevated. If symptoms such as new, severe headache and jaw pain suggest that a person may have this disease, an elevated ESR can increase the suspicion that the disease is present, while a normal ESR argues against this diagnosis. Monitoring an inflammatory condition. When someone has, for example, ESR or CRP (or both tests) help determine how active the disease is and how well treatment is working.

None of these tests is perfect. Sometimes false negative results occur when inflammation actually is present. False positive results may occur when abnormal test results suggest inflammation even when none is present.