Inflammation Pathology Notes


Inflammation Pathology Notes

What is inflammation in pathology notes?

Inflammation is the body’s mechanism for coping with agents that could damage it. In other words, inflammation is a protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces. Although the processes of acute and chronic inflammation are an important protective mechanism used by the body to deal with potentially damaging agents, they are potentially damaging to the body and must be closely regulated.

What are the 5 markers 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,

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.

  • 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.

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. 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.

  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.

  1. Cyclsporin or under development e.g.
  2. NF-κB, p38 MAPK and PDE4 inhibitors,
  3. 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.
  4. 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.
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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.

What are the general characteristics of inflammation?

The cardinal signs of inflammation include: pain, heat, redness, swelling, and loss of function. Some of these indicators can be seen here due to an allergic reaction.
Specialty Immunology, rheumatology
Symptoms Heat, pain, redness, swelling
Complications Asthma, pneumonia, autoimmune diseases
Duration Acute : few days Chronic : up to many months, or years
Causes Infection, physical injury, autoimmune disorder

Inflammation (from Latin : inflammatio ) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators.

  1. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.
  2. The five cardinal signs are heat, pain, redness, swelling, and loss of function (Latin calor, dolor, rubor, tumor, and functio laesa ).

Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g.

bacteria) and compromise the survival of the organism. In contrast, too much inflammation, in the form of chronic inflammation, is associated with various diseases, such as hay fever, periodontal disease, atherosclerosis, and osteoarthritis, Inflammation can be classified as either acute or chronic,

Acute inflammation is the initial response of the body to harmful stimuli, and is achieved by the increased movement of plasma and leukocytes (in particular granulocytes ) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue.

  1. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.
  2. Inflammation has also been classified as Type 1 and Type 2 based on the type of cytokines and helper T cells (Th1 and Th2) involved.

Inflammation is not a synonym for infection, Infection describes the interaction between the action of microbial invasion and the reaction of the body’s inflammatory response—the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction.

Inflammation, on the other hand, describes purely the body’s immunovascular response—whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word urethritis strictly means only “urethral inflammation”, but clinical health care providers usually discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis.

However, the inflammation–infection distinction becomes crucial for situations in pathology and medical diagnosis where inflammation is not driven by microbial invasion, such as the cases of atherosclerosis, trauma, ischemia, and autoimmune diseases (including type III hypersensitivity ).

What is inflammation and its causes?

Inflammation is a process by which your body’s white blood cells and the things they make protect you from infection from outside invaders, such as bacteria and viruses. But in some diseases, like arthritis, your body’s defense system – your immune system – triggers inflammation when there are no invaders to fight off.

In these autoimmune diseases, your immune system acts as if regular tissues are infected or somehow unusual, causing damage. Inflammation can be either short-lived ( acute ) or long-lasting ( chronic ). Acute inflammation goes away within hours or days. Chronic inflammation can last months or years, even after the first trigger is gone.

Conditions linked to chronic inflammation include:

Cancer Heart disease Diabetes Asthma Alzheimer’s disease

Some types of arthritis are the result of inflammation, such as:

Rheumatoid arthritis Psoriatic arthritis Gouty arthritis

Other painful conditions of the joints and musculoskeletal system that may not be related to inflammation include osteoarthritis, fibromyalgia, muscular low back pain, and muscular neck pain, Symptoms of inflammation include:

RednessA swollen joint that may be warm to the touch Joint pain Joint stiffness A joint that doesn’t work as well as it should

Often, you’ll have only a few of these symptoms. Inflammation may also cause flu-like symptoms including:

Fever Chills Fatigue /loss of energy Headaches Loss of appetiteMuscle stiffness

When inflammation happens, chemicals from your body’s white blood cells enter your blood or tissues to protect your body from invaders. This raises the blood flow to the area of injury or infection. It can cause redness and warmth. Some of the chemicals cause fluid to leak into your tissues, resulting in swelling. Your doctor will ask about your medical history and do a physical exam, focusing on:

The pattern of painful joints and whether there are signs of inflammationWhether your joints are stiff in the morningAny other symptoms

They’ll also look at the results of X-rays and blood tests for biomarkers such as:

C-reactive protein (CRP)Erythrocyte sedimentation rate (ESR)

Inflammation can affect your organs as part of an autoimmune disorder. The symptoms depend on which organs are affected. For example:

Inflammation of your heart ( myocarditis ) may cause shortness of breath or fluid buildup.Inflammation of the small tubes that take air to your lungs may cause shortness of breath.Inflammation of your kidneys (nephritis) may cause high blood pressure or kidney failure.

You might not have pain with an inflammatory disease, because many organs don’t have many pain-sensitive nerves. Treatment for inflammatory diseases may include medications, rest, exercise, and surgery to correct joint damage, Your treatment plan will depend on several things, including your type of disease, your age, the medications you’re taking, your overall health, and how severe the symptoms are.

Correct, control, or slow down the disease processAvoid or change activities that aggravate painEase pain through pain medications and anti-inflammatory drugsKeep joint movement and muscle strength through physical therapy Lower stress on joints by using braces, splints, or canes as needed

Medications Many drugs can ease pain, swelling and inflammation. They may also prevent or slow inflammatory disease. Doctors often prescribe more than one. The medications include:

Nonsteroidal anti-inflammatory drugs ( NSAIDs, such as aspirin, ibuprofen, or naproxen )Corticosteroids (such as prednisone)Antimalarial medications (such as hydroxychloroquine )Other medicines known as disease-modifying antirheumatic drugs (DMARDs), including azathioprine, cyclophosphamide, leflunomide, methotrexate, and sulfasalazine Biologic drugs such as abatacept, adalimumab, certolizumab, etanercept, infliximab, golimumab, rituximab, and tocilizumab

Some of these are also used to treat conditions such as cancer or inflammatory bowel disease, or to prevent organ rejection after a transplant. But when ” chemotherapy ” types of medications (such as methotrexate or cyclophosphamide) are used to treat inflammatory diseases, they tend to have lower doses and less risk of side effects than when they’re prescribed for cancer treatment,

Quit smoking,Limit how much alcohol you drink.Keep a healthy weight, Manage stress,Get regular physical activity,Try supplements such as omega-3 fatty acids, white willow bark, curcumin, green tea, or capsaicin, Magnesium and vitamins B6, C, D, and E also have some anti-inflammatory effects. Talk with your doctor before starting any supplement.

Surgery You may need surgery if inflammation has severely damaged your joints. Common procedures include:

Arthroscopy. Your doctor makes a few small cuts around the affected joint. They insert thin instruments to fix tears, repair damaged tissue, or take out bits of cartilage or bone, Osteotomy. Your doctor takes out part of the bone near a damaged joint. Synovectomy. All or part of the lining of the joint (called the synovium) is removed if it’s inflamed or has grown too much. Arthrodesis, Pins or plates can permanently fuse bones together. Joint replacement. Your doctor replaces a damaged joint with an artificial one made of metal, plastic, or ceramic.

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The things you eat and drink can also play a role in inflammation. For an anti-inflammatory diet, include foods like:

Tomatoes Olive oilLeafy green vegetables (spinach, collards)Nuts (almonds, walnuts)Fatty fish ( salmon, tuna, sardines)Fruits (berries, oranges )

These things can trigger inflammation, so avoid them as much as you can:

Refined carbohydrates (white bread )Fried foods (French fries)Sugary drinks (soda)Red and processed meats (beef, hot dogs)Margarine, shortening, and lard

What are positive markers of inflammation?

How this fits in – There is a lack of research comparing the accuracy of inflammatory markers. Testing multiple inflammatory markers is common, leading to concerns about overuse. In this large observational study using UK primary care electronic health records the authors found very little difference between the accuracy of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and plasma viscosity (PV).

What is a high inflammatory marker?

What is a c-reactive (CRP) protein test? – A c-reactive protein test measures the level of c-reactive protein (CRP) in a sample of your blood. CRP is a protein that your liver makes. Normally, you have low levels of c-reactive protein in your blood. Your liver releases more CRP into your bloodstream if you have inflammation in your body.

High levels of CRP may mean you have a serious health condition that causes inflammation. Inflammation is your body’s way of protecting your tissues and helping them heal from an injury, infection, or other disease. Inflammation can be acute (sudden) and temporary. This type of inflammation is usually helpful.

For example, if you cut your skin, it may turn red, swell, and hurt for a few days. Those are signs of inflammation. Inflammation can also happen inside your body. If inflammation lasts too long, it can damage healthy tissues. This is called chronic (long-term) inflammation.

Chronic infections, certain autoimmune disorders, and other diseases can cause harmful chronic inflammation. Chronic inflammation can also happen if your tissues are repeatedly injured or irritated, for example from smoking or chemicals in the environment. A CRP test can show whether you have inflammation in your body and how much.

But the test can’t show what’s causing the inflammation or which part of your body is inflamed. Other names: c-reactive protein, serum

What is a positive inflammatory marker?

Blood tests known as ‘inflammatory markers’ can detect inflammation in the body, caused by many diseases including infections, auto-immune conditions and cancers. The tests don’t identify what’s causing the inflammation: it might be as simple as a viral infection, or as serious as cancer.

What is histology of inflammation?

OVERVIEW CARDINAL SIGNS (the “four ORs:” rubor, tumor, calor, dolor ) PHYSIOLOGY

Increased perfusion Increased permeability Emigration of leukocytes Neural response


Neutrophils Lymphocytes and plasma cells Monocytes Eosinophils

Examples of inflammation in skin and overview of lymphatic system, Microscopically, inflammation shows up most clearly as increased numbers of white blood cells ( i.e., the inflammatory infiltrate which results from emigration of leukocytes ). Recent Research

OVERVIEW The inflammatory response is very familiar. TRY IT YOURSELF : A mild example can be produced at your convenience. Without breaking the surface, firmly scrape the skin on your forearm; then watch as redness (with possibly some mild swelling and heat) develops over the next few minutes.

Inflammation is characterized by several familiar signs: redness, swelling, heat and pain, To understand inflammation is to understand how and why these signs develop. These signs represent a response that is programmed into your tissue. This response is one of your body’s principal defense reactions, designed to anticipate, intercept and destroy invading microorganisms.

Inflammation is best appreciated by understanding your body’s functioning at the level of cells and tissues. Subsequent processes of tissue repair (healing) involve cell growth and division, cell movement and differentiation, and manufacture of extracellular material.

We go through life separated from our environment by a cellular boundary. This boundary – including the epidermis of our skin and the epithelia of our various mucous membranes – covers all our body’s surfaces, even the internal surfaces of lungs, gut and glandular ducts. Nothing enters or leaves the body except by passing through or between the cells which form this epithelial boundary,

Whenever this epithelial boundary is broken, as it often is by scrapes and cuts and insect bites, two unfortunate things can happen. Good stuff like blood can leak out. And bad stuff like germs (microorganisms) can creep in. Plugging the leak can be fairly straightforward, with a quick patch (a blood clot) preventing significant loss of bodily substance.

  1. But a quick patch is not enough to prevent serious infection.
  2. Because germs are alive, they can grow and proliferate.
  3. So even a few microbes invading your body at the moment of injury could, if left unmolested, rapidly convert your warm, moist, well-oxygenated tissues into a thriving bacterial culture.

Inflammation helps avoid this result. Unfortunately, inflammation is uncomfortable. And inflammation can sometimes be triggered inappropriately (e.g., by allergies or autoimmune diseases). Many common medical treatments (e.g., aspirin and other “anti-inflammatory agents”) are intended to relieve the discomfort and/or reduce the attendant tissue disturbance that inflammation may cause.

Any organ can become inflamed. Inflammation of a particular body part is named according to the site, with the “- itis ” suffix appended (e.g., tonsillitis, appendicitis, dermatitis, arthritis, sinusitis, etc.). Thus many disease names are really just words that identify sites of inflammation. Nevertheless, inflammation is largely a function of connective tissue,

The most typical histological sign of inflammation is the accumulation of white blood cells within connective tissue. Tissue repair, Following inflammation, injured tissue is usually replaced by new cells and extracellular materials, with undamaged surrounding cells proliferating and migrating to fill the void.

  1. Although some tissues, especially surface epithelium, can grow back quite efficiently, complex organization is seldom matched in the regenerated site.
  2. Gaps are quickly filled by collagen fibers produced by proliferating fibroblasts,
  3. A mass of collagen which replaces tissue that has been destroyed is known as a scar,

Scars in the skin appear white because collagen is colorless, and healing often creates a more compact arrangement of collagen with fewer capillaries than the surrounding tissue. Scars in other organs also exist as firm masses of collagen in which normal organ function cannot occur.

Rubor – redness. Tumor – swelling (puffiness, edema ). Calor – heat. Dolor – pain. (A fifth sign, loss of function, is sometimes included in this list.)

Where do these signs come from? What is happening to your body during inflammation? As you understand inflammation, you should be able to answer the following specific questions.

Why does tissue become red and warm around a site of injury? Why does inflamed tissue swell? What is pus, and how does it form? How does healing occur?

TOP OF PAGE PHYSIOLOGY OF INFLAMMATION The four cardinal signs of inflammation are readily explained by the behavior of the underlying cells and tissues. The inflammatory response consists of several physiological processes, all of which are triggered by the release of pharmacologically active substances such as histamine and heparin,

Vasodilation Increased vascular permeability Emigration of white blood cells

Vasodilation ( increased vascular perfusion ).

Relaxation of the smooth muscle which surrounds terminal arterioles results in increased blood flow into the connective tissue capillary bed. Increased tissue perfusion in turn causes redness ( rubor ), as more red blood cells pass through the tissue, and warmth ( calor ), as blood carries body heat from the body’s core to cooler peripheral tissues.

Increased vascular permeability (see Webpath ).

The endothelial lining of capillaries ( endo = inside; the endothelium is the layer of thin, flat cells which line blood vessels ) becomes more leaky, allowing more fluid (blood plasma) to exude into the connective tissue spaces. There is normally a balance between fluid leaving vascular spaces and fluid re-entering the system. Inflammation shifts this balance, causing accumulation of interstitial fluid. The fluid build-up which follows this permeability change is called edema and is visible as puffiness or swelling ( tumor ).

Note that edema can take a variety of forms, from mild (e.g., a blister) to life-threatening. Emigration of leukocytes (see Webpath ).

Vasodilation and increased vascular perfusion are designed to prepare the way for the inflammatory infiltrate to enter the inflamed tissue. A combination of vasodilation with thickening of the blood (due to fluid leaking out of the vessels) causes a slowing of flow rate, which encourages leukocytes (white blood cells; leuko = white, cyte = cell) to stick to the sides of the vessels. This is called “margination” or “pavementing” (the white blood cells gather along the endothelium, like bricks paving a road). From here the leukocytes crawl between the endothelial cells and enter the inflamed connective tissue. Increased metabolic activity associated with leukocyte activity also generates heat ( calor ), contributing to local warmth.

Pain and/or itching ( dolor ) is caused by direct action on nerve endings of the chemical agents released during inflammation. TOP OF PAGE INFLAMMATORY INFILTRATE ( Introduction to inflammation ) The inflammatory or leukocytic infiltrate consists of white blood cells which leave the blood and enter (infiltrate) the inflamed connective tissue

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Images of inflammatory infiltrate in skin, Inflammatory infiltrate in salivary gland, from Webpath, Inflammatory infiltrate in nasal mucosa, from Webpath,

Cells of the inflammatory infiltrate include neutrophils, lymphocytes and monocytes, Immigration of these cells into peripheral tissues is one of the principal purposes for inflammation, bringing to a site of injury the immune-system cells which can combat infection and clean up damaged tissue. Neutrophils (neutrophilic leukocytes) are the first white blood cells to enter the tissue during acute inflammation (see Webpath ). Neutrophils are anti-bacterial cells which lyse (break down) bacterial cells by releasing lysosomal enzymes. Neutrophils recognize bacteria as foreign by the antibody molecules which have attached to the bacterial surface.

  • Antibody molecules (molecules which bind to one specific antigen or foreign substance which the body has previously encountered) are found in blood plasma and interstitial fluid.
  • Neutrophils are the most numerous of the leukocytes, about 60% of the white blood cell count.
  • They are about 12 m in diameter in blood smear preparations (about twice the size of red blood cells), and are polymorphonuclear (meaning their nuclei have a variable shape with several lobes; neutrophils are also called PMNs or polys, short for polymorphonuclear neutrophilic leukocytes).

The cytoplasm contains many lysosomal granules (vesicles storing lysosomal enzymes) whose specific staining properties give these cells their name. The granules are neutrophilic, meaning they do not show a special affinity for either acidic or basic stains, but are stained mildly by both.

This is in contrast to the specific granules of eosinophils, which stain red with eosin, and basophils, which stain with basic stains. Severe inflammation may increase the numbers of neutrophils in blood, resulting in neutrophilia Neutrophils are only occasionally seen in tissue sections outside blood (except, of course, in inflamed tissue).

Here they may be most easily recognized by their lobed nuclei. One neutrophil nucleus might be mistaken for a cluster of very small nuclei, but each of the lobes is much smaller than any whole nucleus-only two or three m across, much smaller than the nuclei of lymphocytes which are among the smallest of our cells. Lymphocytes accumulate somewhat later during the inflammatory process. Their presence in large numbers indicates the continuing presence of antigen and thus may suggest an established infection. Lymphocytes produce the multitude of diverse antibody molecules (one specific type of antibody per lymphocyte) which provide the mechanism for chemical recognition of foreign materials (distinguishing between self and non-self) and so for mediating and regulating immune responses.

Lymphocytes travel in the blood, but they routinely leave capillaries and wander through connective tissue. Therefore, lymphocytes may be normally encountered at any time in any location. They even enter epithelial tissue, crawling between the epithelial cells. They reenter circulation via lymphatic system channels (hence their name).

Lymph channels drain into lymph nodes, where dense aggregations of lymphocytes form lymph nodules, Each lymph nodule has a “germinal center”, where activated lymphocytes proliferate. Lymph nodules with proliferating lymphocytes also characterize the tonsils and the appendix and may be encountered in other sites as well.

  • Research suggests that some types of lymphocytes are compartmentalized to particular tissues or body regions.
  • Lymphocytes are small cells, 7-9 m in diameter in blood smears, and are the second most common white blood cell type (about 30% of the WBCs).
  • Each lymphocyte has a round heterochromatic (deeply staining) nucleus surrounded by a relatively thin rim of cytoplasm.

Lymphocytes are most easily recognized in histological sections as small “naked” nuclei (the cytoplasm is usually inconspicuous) which occur here and there in most ordinary connective tissues. They are encountered most commonly near mucous membranes. Lymphocytes are found densely packed in lymphoid tissue, such as tonsils, spleen, and lymph nodes.

  • Plasma cells are lymphocytes which are specialized for mass production and secretion of circulating antibodies.
  • Plasma cells have more extensive cytoplasm filled with rough endoplasmic reticulum (for synthesizing protein, specifically antibody molecules).
  • This cytoplasm is distinctly basophilic, a consequence of the large numbers of ribosomes associated with the rER, and typically forms a lopsided bulge on one side of the nucleus.

The heterochromatin of plasma cells is typically clumped in a characteristic “spoke-wheel” arrangement which also aids plasma cell recognition. Monocytes are phagocytic cells which circulate in the blood. An equivalent cell type, called the macrophage, is a resident cell in connective tissue.

Monocytes/macrophages engulf and digest foreign microorganisms, dead or worn-out cells, and other tissue debris. They interact closely with lymphocytes to recognize and destroy foreign substances. Resident macrophages normally remain at rest (rather than circulating in and out of tissues like the lymphocytes).

But the normal number of fixed macrophages is supplemented during inflammation by the influx of many monocytes from the blood. When faced with a target too big for one cell, a splinter for example, several macrophages may fuse together to form a single huge multinucleate mass called a “foreign body giant cell.” Monocytes are the largest of the leukocytes, and constitute about 5% of the white blood cell population.

  1. In blood smears, monocyte nuclei are typically indented, with a kidney-bean shape.
  2. Tissue macrophages are diverse in appearance and not easily distinguished from the more common fibroblasts.
  3. Macrophages are generally larger, and may contain brown pigment granules which represent indigestible residue in tertiary lysosomes.

In electron micrographs macrophages are generally recognized by the presence of numerous lysosomes of various sizes, including large heterophagic vesicles. Eosinophils are circulating white blood cells which may extravasate and accumulate in connective tissue in association with allergy and parasite infection.

“The spectrum of inflammatory responses” (vol.374, p.1070). “Dying cells fan the flames of inflammation” (vol.374, p.1076). “Mechanisms of viral inflammation and disease in humans” (vol.374, p.1080). “Signaling inflammation across the gut-brain axis” (vol.374, p.1087).

What is type 2 inflammation pathology?

From Wikipedia, the free encyclopedia Type 2 inflammation is a pattern of immune response, Its physiological function is to defend the body against helminths, but a dysregulation of the type 2 inflammatory response has been implicated in the pathophysiology of several diseases.

What is the most important feature of inflammation?

The most important feature of inflammation is the accumulation of white blood cells at the site of injury. Most of these cells are phagocytes, certain “cell-eating” leukocytes that ingest bacteria and other foreign particles and also clean up cellular debris caused by the injury.

The main phagocytes involved in acute inflammation are the neutrophils, a type of white blood cell that contains granules of cell-destroying enzymes and proteins. When tissue damage is slight, an adequate supply of these cells can be obtained from those already circulating in the blood. But, when damage is extensive, stores of neutrophils—some in immature form—are released from the bone marrow, where they are generated.

To perform their tasks, not only must neutrophils exit through the blood vessel wall but they must actively move from the blood vessel toward the area of tissue damage. This movement is made possible by chemical substances that diffuse from the area of tissue damage and create a concentration gradient followed by the neutrophils.

  • The substances that create the gradient are called chemotactic factors, and the one-way migration of cells along the gradient is called chemotaxis,
  • Large numbers of neutrophils reach the site of injury first, sometimes within an hour after injury or infection.
  • After the neutrophils, often 24 to 28 hours after inflammation begins, there comes another group of white blood cells, the monocytes, which eventually mature into cell-eating macrophages,

Macrophages usually become more prevalent at the site of injury only after days or weeks and are a cellular hallmark of chronic inflammation.

What is the concept of inflammation?

(IN-fluh-MAY-shun) A normal part of the body’s response to injury or infection. Inflammation occurs when the body releases chemicals that trigger an immune response to fight off infection or heal damaged tissue. Once the injury or infection is healed, the inflammatory process ends.

What is the definition of inflammation?

(IN-fluh-MAY-shun) A normal part of the body’s response to injury or infection. Inflammation occurs when the body releases chemicals that trigger an immune response to fight off infection or heal damaged tissue. Once the injury or infection is healed, the inflammatory process ends.

What does inflammatory mean in medical terms?

(in-FLA-muh-TOR-ee) Having to do with inflammation (redness, swelling, pain, and a feeling of heat that helps protect tissues affected by injury or disease ).

What is inflammation and infection short note?

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’.

What is the term for inflammation?

1 : a local response to cellular injury that is marked by capillary dilatation, leukocytic infiltration, redness, heat, and pain and that serves as a mechanism initiating the elimination of noxious agents and of damaged tissue