Inflammation mediators (2022)


inflammation, reaction of the body to injury or to infectious, allergic, or chemical irritation. The symptoms are redness, swelling, heat, and pain resulting from dilation of the blood vessels in the affected part with loss of plasma and leucocytes (white blood cells) into the tissues. White blood cells communicate with each other via cytokines, which are polypeptides released by cells of the immune system that regulate other cells. They are a broad class of soluble compounds that signal one cell type to another, particularly in response to foreign substances. Granulomas are most common in infectious diseases such as tuberculosis, leishmaniasis, and schistosomiasis, in which the body's defenses, unable to destroy the offending organisms, try to enclose them in a mass of inflammatory cells. Certain types of inflammation result in pus formation, as in an abscess. The leukocytes destroy harmful microorganisms and dead cells, preventing the spread of the irritation and permitting the injured tissue to repair itself.

The Columbia Electronic Encyclopedia™ Copyright © 2022, Columbia University Press. Licensed from Columbia University Press. All rights reserved.

The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.

(Video) Mediators of Inflammation: An Introduction


a complex defense reaction of the body for dealing with harmful agents developed in the course of evolution and manifested by various vascular and tissue changes. Inflammation is one of the processes underlying many diseases with different clinical symptoms. The biological role of inflammation is to limit the spread of pathogenic agents in the body; sometimes the inflammatory process helps to destroy them. Intensive study of the mechanisms of inflammation began after R. Virchow advanced his theory of cellular pathology. According to this theory, inflammation is a local tissue reaction morphologically manifesting itself in protein dystrophy of cells. The German scientist J. Konheim regarded disturbances in the flow of blood and lymph in the inflammatory focus as the primary factor in inflammation. The Russian biologist E. Metchnikoff developed a fundamentally new approach to the analysis of inflammation with his general biological theory (1892) based on the results of a comparative pathological study of the process. Metchnikoff demonstrated the decisive significance of evolutionary characteristics and perfection of the organism in the development of inflammation. He also described phagocytosis as an inseparable part of the inflammatory process and scientifically substantiated the relationship between a focus of inflammation and the body as a whole.

The causes of inflammation may be either exogenous (external), such as bacteria and their toxins, mechanical injury, effects of radiation or electrical energy, and chemical substances, or endogenous (arising within the organism itself), including products of tissue necrosis and decomposition, thrombi, infarcts, hematomas, and deposits of salts. Depending on the course, inflammation may be acute, subacute, or chronic. An acute inflammation of the skin, such as an abscess or burn, is manifested by redness, swelling, elevated temperature in the area of inflammation, soreness, and functional impairment of the affected organs and tissues. Not all of the above symptoms are present in chronic inflammation or in inflammation of the internal organs.

(Video) Inflammatory Mediators

Inflammation consists of a vascular reaction, alteration, and proliferation. The vascular reaction is manifested first by a transient vascular spasm in the inflammatory focus followed by dilation of the arterioles and capillaries, which undergo an intensified filling with blood (arterial hyperemia). The external signs are elevated temperature in the focus, redness, and pulsation. These vascular changes are due to an accumulation in the inflammatory focus of substances that affect the tone of the vascular wall, such as acetylcholine, histamine, and adenine nucleotides. The next phase of the vascular changes involves dilation of the venous network and slowing of the blood flow. Because of an increased permeability of the vascular walls, plasma (the liquid part of the blood) and leukocytes (exudation) emerge into the surrounding tissues. The causative agent of the inflammation greatly affects the nature of the exudative process and composition of the exudate (inflammatory effusion). The exudate can be serous (from serum), fibrinous (with an increased amount of protein), leukocytic (with many leukocytes), purulent, or hemorrhagic (with many erythrocytes). The exudate causes the swelling of tissues in the focus of inflammation. It can accumulate in cavities, for example, in pleuritis. Pain is caused by compression of the edema and by irritation of the nerve endings in the inflammatory focus by the metabolic products. During the vascular changes the leukocytes approach the vascular wall (phenomenon of margination of leukocytes), after which they emerge from the vascular stream (diapedesis) and migrate to the focus of inflammation. Here they carry out phagocytosis. The migration of leukocytes to the focus is caused by chemotaxis (drawing of leukocytes from the blood by chemical agents accumulating in the inflammatory focus), by the appearance in the inflammatory focus of substances capable of decreasing the surface tension of leukocytes and of substances that convert leukocyte protoplasm from a sol to a gel, and by electrokinetic factors.

Circulatory disturbances in a focus of inflammation are accompanied by the development of thrombi and protein coagula (protein flakes) in the blood vessels and lymphatics, by the filling of their lumens with various cellular elements that enter the exudate in profusion, and by increased vascular tone and compression of the small vessels by edema. These processes eventually block the efferent blood vessels and lymphatics, thus making it difficult for bacteria and the toxic products formed by tissue breakdown to become absorbed and enter the bloodstream; that is, the focus of inflammation is separated from healthy tissue. The presence of a greater or lesser admixture of multiplying mesenchymal cells stimulates the subsequent regenerative processes in the injured tissues.

Alteration (lesion) of tissues in inflammation is reflected in structural and functional changes in the injured tissue. The tissue changes range from dystrophy (protein, fatty, and hyaline) to necrosis (death) of tissues, and they are the result of nutritional and metabolic disorders. All the metabolic processes (the “fire of metabolism”) are sharply intensified and qualitatively changed in a focus of inflammation. Glucose is excessively consumed in inflamed tissue at a time when the oxygen is relatively inadequate. Moreover, the respiratory coefficient decreases and anaerobic glycolysis intensifies. The accumulation of lactic acid and other incompletely oxidized metabolic products produces acidosis, fatty acids increase, and the content of ketone bodies increases in blood flowing from the focus. In the inflamed tissue protein decomposition also intensifies. The metabolic disturbances give rise to increased osmotic and oncotic pressure in the focus.

Proliferation (multiplication of cellular elements) takes place on the periphery of a focus of inflammation against a background of exudation and alteration processes, and it is most pronounced in the final stages of the process. Proliferation is followed by gradual regeneration (repair of tissues), which completes the inflammatory process. Inflammation may be exudative, alterative, or proliferative, depending on the particular component that is dominant. Inflammation always results in the death of tissues. The outcome of the inflammation depends on the condition of the body, the form of inflammation, and the size of the focus. Inflammation may be normergic (characteristic of a healthy body) or hyperergic, when the body is sensitized. The latter form is characterized by intensive alteration, for example, Pirquet’s reaction. Hypoergic inflammation occurs in the presence of immunity to the factor that caused the inflammation and when the body is exhausted. Development of the inflammatory process is also largely a function of age, nutrition, and metabolism. The nervous and endocrine systems play a major role in the development of inflammation. Excitation of the sympathetic nervous system decreases the inflammatory phenomena, while excitation of the parasympathetic nervous system intensifies them. Hormones also influence the course of inflammation in different ways. Thus, the adenocorticotropic hormone (ACTH) of the hypophysis and the glucocorticoids of the suprarenal gland inhibit the development of inflammation while the mineralocorticoids of the suprarenal gland activate it. Dysfunction of the pancreas (diabetes mellitus) causes a predisposition to stubborn pyoderma. Inflammation is severe with increased thyroid function (hyperthyroidism). Small thrombi and dead tissues are resorbed in the final stage of inflammation (enzymic splitting, phagocytosis). The large defects formed in the tissues as a result of fibrinous-necrotic inflammation are replaced by scar tissue, which impairs the function of organs (for example, cirrhosis of the liver after hepatitis) and deforms them (for example, deformity of the heart valves after endocarditis). Inflammation of the tubular organs (esophagus, uterine tubes, intestines) may result in their becoming constricted and their lumens closing completely (obliteration). When the exudate is resorbed from the body cavities (abdominal, pleural, and others), the fibrin remaining on the surface of the serous membranes forms adhesions.

(Video) INFLAMMATION Part 4: Chemical Mediators- HISTAMINE & SEROTONIN

Inflammation may provoke a greater or lesser reaction throughout the body, depending on where it originates and on the size of the focus. The body mobilizes its defensive forces and creates antibodies. Moreover, symptoms of intoxication (poisoning) may appear when the products of the vital activity of the causative agents and the products of tissue decomposition are resorbed. They include chiefly fever, an increased number of leukocytes in the peripheral blood (leukocytosis), and an accelerated erythrocyte sedimentation rate (ESR). When the bacteria are carried to parts of the body remote from the focus of inflammation, metastatic inflammatory foci may arise.


Al’pern, D. E. Vospalenie (Voprosy patologii). Moscow, 1959.
Metchnikoff, E. Lektsii o sravnitel’noi patologii vospaleniia. Moscow, 1947.
Menkin, V. Dynamics of Inflammation. New York, 1940.


(Video) Immunology - Mediators of Inflammation

The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.




Local tissue response to injury characterized by redness, swelling, pain, and heat.

(Video) Acute Inflammation | symptoms |Pathogenesis, Cause of inflammation| Mediators of Acute Inflammation.

McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.


the reaction of living tissue to injury or infection, characterized by heat, redness, swelling, and pain

Collins Discovery Encyclopedia, 1st edition © HarperCollins Publishers 2005


What are the mediators of inflammation? ›

The released chemical mediators include (1) vasoactive amines such as histamine and serotonin, (2) peptide (e.g., bradykinin), and (3) eicosanoids (e.g., thromboxanes, leukotrienes, and prostaglandins).

What are the 5 inflammatory responses? ›

There are five fundamental signs of inflammation that include: heat (calor), redness (rubor), swelling (tumor), pain (dolor), and loss of function (functio laesa).

What purpose do mediators of inflammation serve? ›

An inflammatory mediator is a messenger that acts on blood vessels and/or cells to promote an inflammatory response.

What are three primary goals of the inflammatory response? ›

The primary goal of the inflammatory response is to detect and eliminate factors that interfere with homeostasis. A typical inflammatory response consists of four components: inflammatory inducers; the detecting sensors; downstream mediators; and the target tissues that are affected.

Which mediators of inflammation causes pain? ›

The pain associated with inflammation results in part from the distortion of tissues caused by edema, and it also is induced by certain chemical mediators of inflammation, such as bradykinin, serotonin, and the prostaglandins.

What does mediator mean? ›

Definition of mediator

1 : one that mediates especially : one that mediates between parties at variance. 2 : a mediating agent in a physical, chemical, or biological process.

What are the 4 main signs of inflammation? ›

This type of stimulation–response activity generates some of the most dramatic aspects of inflammation, with large amounts of cytokine production, the activation of many cell types, and in fact the four cardinal signs of inflammation: heat, pain, redness, and swelling (1).

Does coffee cause inflammation? ›

Coffee may help reduce inflammation in most people. However, some people may experience increased inflammation following coffee consumption. If this applies to you, consider reducing your intake.

What activates inflammatory response? ›

The inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause. The damaged cells release chemicals including histamine, bradykinin, and prostaglandins. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling.

Where do pain mediators come from? ›

Following tissue injury, pain signals and inflammatory mediators are released by peripheral afferent sensory fibers and act on the post-synaptic membrane to cause stimulation of nociceptive neurons and the perception of pain by the central nervous system [4].

Why does the body cause inflammation? ›

When your body activates your immune system, it sends out inflammatory cells. These cells attack bacteria or heal damaged tissue. If your body sends out inflammatory cells when you are not sick or injured, you may have chronic inflammation.

Which group of mediators initiates the inflammatory response? ›

Neutrophils are key mediators of the inflammatory response, and program antigen presenting cells to activate T cells and release localized factors to attract monocytes and dendritic cells [7].

What mechanism usually regulates the inflammatory response? ›

The inflammatory response is naturally regulated by a variety of endogenous factors, including IL-10 and IL-13. These ILs suppress the inflammatory response by blocking activation of NF-κB.

What are the 3 stages of inflammatory response? ›

The are three main stages of inflammation which can each vary in intensity and duration: Acute -swelling stage. Sub-acute – regenerative stage. Chronic – scar tissue maturation and remodelling stage.

How does inflammation resolve? ›

Mediators released early in inflammation, like ACTH, can also enable the induction of the pro-resolving phase. Upon activation, neutrophils release microparticles containing pro-resolution mediators that control further granulocyte ingress and turn on a resolution and tissue reparative programs.

Is histamine an inflammatory mediator? ›

Histamine is a potent inflammatory mediator, commonly associated with allergic reactions, promoting vascular and tissue changes and possessing high chemoattractant activity.

What are mediators in the body? ›

Mediators can be defined as compounds that are either locally released or carried in blood or tissue fluids and that may participate in initiating, perpetuating, or aggravating a pathological process.

What are immune mediators? ›

Cytokines are the mediators of the immune system. They are small proteins of around 25 kD that are produced in response to a stimulus (ie, invading microbes) by numerous cell types.

What are the 3 types of mediation? ›

Much like doctors and counselors will use different strategies to achieve desired results, so too do mediators use different techniques. The three main styles of mediation are evaluative, facilitative, and transformative.

What is the main purpose of mediation? ›

Even if disputants do not resolve the dispute, mediation frequently will "bring out" the real issues and enhance communications between the parties, fostering an improved working relationship.

What is mediation with example? ›

The definition of mediation is a process of negotiation in a relationship to resolve differences. When a couple is divorcing and they work with a neutral third party that helps them resolve divorce issues and divide up assets and property, this is an example of mediation.

Does sugar cause inflammation? ›

Consuming too much added sugar can raise blood pressure and increase chronic inflammation, both of which are pathological pathways to heart disease.

Does stress cause inflammation? ›

Research shows that stress can cause inflammation in the body, leading to a number of chronic health conditions.

Are eggs inflammatory? ›

Consuming eggs regularly can lead to an increased amount of swelling and joint pain. The yolks contain arachidonic acid, which helps trigger inflammation in the body. Eggs also contain saturated fat which can also induce joint pain.

Is oatmeal an inflammatory food? ›

on Inflammation: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Background: Oat and its compounds have been found to have anti-inflammatory effects.

Are eggs anti-inflammatory? ›

Are eggs an anti-inflammatory food? Yes. Eggs are a source of vitamin D, which has anti-inflammatory effects. 10 They're also a good source of protein and B vitamins.

Which cells play a role in inflammation? ›

Pro-inflammatory cytokines
  • IL-1β is released primarily by monocytes and macrophages as well as by nonimmune cells, such as fibroblasts and endothelial cells, during cell injury, infection, invasion, and inflammation. ...
  • IL-6 has been shown to play a central role in the neuronal reaction to nerve injury.

When does inflammation peak? ›

Phase 2: Inflammation (swelling)

Inflammation starts within the first hour or two after injury, peaks within 1-3 days but lasts at least a couple of weeks. This phase is when you will experience swelling and some heat around your injury. This is entirely normal and a natural part of your body's tissue healing process.

How do you reduce neuroinflammation? ›

Integrated therapies that include drug therapy as well as mind/body and plant-based therapies will likely be the most successful approach for reducing neuroinflammation and ameliorating CNS dysfunction.

What causes the release of inflammatory mediators? ›

Inflammatory mediators important in OM are produced by infiltrating immune cells such as neutrophils, monocytes, and lymphocytes. In addition, local cells such as keratinocytes and mast cells have been shown to produce inflammatory mediators.

Is histamine a pain mediator? ›

Histamine is a key mediator in the processing of nociceptive information, acting in an antinociceptive manner in the CNS while, conversely, in a nociceptive manner in the PNS (Khalilzadeh, Azarpey, Hazrati, & Vafaei Saiah, 2018).

Which chemical is responsible for pain? ›

Chemical substances produced by the body that excite pain receptors include bradykinin, serotonin, and histamine. Prostaglandins are fatty acids that are released when inflammation occurs and can heighten the pain sensation by sensitizing the nerve endings; that increase in sensitivity is called hyperalgesia.

Do tomatoes cause inflammation? ›

Some people feel that eating foods from the nightshade family, also known as solanaceous vegetables, may make their arthritis worse. But research has shown that there is no link between inflammation and solanaceous vegetables. Examples of nightshade vegetables include: Tomatoes.

Does inflammation raise blood pressure? ›

Background. Inflammation is associated with elevated blood pressure (BP) in the general population [1, 2]. In rheumatoid arthritis (RA), the levels of inflammation, as measured by C-reactive protein (CRP) can be 10-fold higher than in the general population.

Why does the immune system cause inflammation? ›

When an injury occurs, the cells of our immune system immediately travel to the site of injury or irritation and the inflammatory response begins. This includes widening of local blood vessels to allow fluid and immune cells into surrounding injured tissue, which causes swelling, redness, warmth and pain at the site.

What are the two most common mediators of inflammation and their role quizlet? ›

Histamine and serotonin are critical mediators of inflammatory responses because they are preformed (located in granules) and are released rapidly and early during inflammation.

What other cells and mediators play a role in acute inflammation? ›

Other cells that may mediate acute inflammation include epithelial cells and lymphocytes. This chapter reviews the key functions of these cells in response to an acute insult. Keywords: Cytokines, Inflammation, Innate immunity, Macrophages, Mast cells, Monocytes, Neutrophils, Phagocytosis.

Are cytokines inflammatory mediators? ›

Inflammatory Cytokines review

Inflammation, the response of tissue to injury, is characterized in the acute phase by increased blood flow and vascular permeability along with the accumulation of fluid, leukocytes, and inflammatory mediators such as cytokines.

How do inflammatory mediators cause insulin resistance? ›

AT inflammation may contribute to local (AT) and systemic insulin resistance through autocrine effects of inflammatory cells/molecules on insulin signaling and metabolism in adipocytes and endocrine effects of inflammatory molecules secreted by AT (known as adipokines) on insulin sensitivity in other tissues, ...

Does high insulin cause inflammation? ›

As type 2 diabetes starts to develop, the body becomes less sensitive to insulin and the resulting insulin resistance also leads to inflammation. A vicious cycle can result, with more inflammation causing more insulin resistance and vice versa.

What happens first in inflammation? ›

Acute inflammation starts after a specific injury that will cause soluble mediators like cytokines, acute phase proteins, and chemokines to promote the migration of neutrophils and macrophages to the area of inflammation.

Does inflammation cause pain? ›

Acute inflammation can cause pain of varying types and severity. Pain may be constant and steady, throbbing and pulsating, stabbing, or pinching. Pain results when the buildup of fluid leads to swelling, and the swollen tissues push against sensitive nerve endings.

When does the inflammatory phase begin? ›

Introduction to Wound Management

The inflammatory phase is the immediate response to the trauma and sets about preparing the groundwork for the remaining two phases. The wound swells and there is the inevitable bleeding which is a primary mechanism through which debris and toxins can be removed.

What is chronic inflammation? ›

Chronic inflammation is also referred to as slow, long-term inflammation lasting for prolonged periods of several months to years. Generally, the extent and effects of chronic inflammation vary with the cause of the injury and the ability of the body to repair and overcome the damage.

How is acute inflammation terminated? ›

Inflammation is terminated when the offending agent is eliminated. The reaction resolves rapidly, because the mediators are broken down and dissipated and the leukocytes have short life spans in tissues.

Which cells and cell mediators are involved in inflammation? ›

The inflammatory response involves a highly coordinated network of many cell types. Activated macrophages, monocytes, and other cells mediate local responses to tissue damage and infection.

Are cytokines inflammatory mediators? ›

Inflammatory Cytokines review

Inflammation, the response of tissue to injury, is characterized in the acute phase by increased blood flow and vascular permeability along with the accumulation of fluid, leukocytes, and inflammatory mediators such as cytokines.

Is histamine an inflammatory mediator? ›

Histamine is a potent inflammatory mediator, commonly associated with allergic reactions, promoting vascular and tissue changes and possessing high chemoattractant activity.

What are cell mediators? ›

These mediators include histamine, neutral proteases, proteoglycans, and some cytokines, such as tumor necrosis factor-alpha (TNF-alpha). They are responsible for many of the acute signs and symptoms of mast cell-mediated allergic reactions, including edema, bronchoconstriction, and increased vascular permeability.

Where are inflammatory mediators located? ›

Sources of inflammatory mediators

In addition, local cells such as keratinocytes and mast cells have been shown to produce inflammatory mediators. It is also coming to light that besides the middle ear, the inner ear tissues are able to produce inflammatory cytokines and use NF-κB activation (6).

What is the main cause of inflammation in the body? ›

Possible Causes

The most common reasons for chronic inflammation include: Autoimmune disorders, such as lupus, where your body attacks healthy tissue. Exposure to toxins, like pollution or industrial chemicals. Untreated acute inflammation, such as from an infection or injury.

What is the main inflammatory cell? ›

The predominant cell of acute inflammation is the neutrophil. They are attracted to the site of injury by the presence of chemotaxins, the mediators released into the blood immediately after the insult.

What three cytokines play a major role in inflammation? ›

The key pro-inflammatory cytokines are IL-1, IL-6, and TNF-α. These cytokines signal via type I cytokine receptors (CCR1) that are structurally divergent from other cytokine receptor types. They are crucial for coordinating cell mediated immune response and play a critical role in modulating the immune system.

What immune cells release cytokines? ›

Cytokines are mainly produced by macrophages and lymphocytes, although they can also be produced by polymorphonuclear leukocytes (PMN), endothelial and epithelial cells, adipocytes, and connective tissue. Cytokines are essential to the functions of macrophages.

Which immune cells produce cytokines? ›

Cytokines are made by many cell populations, but the predominant producers are helper T cells (Th) and macrophages. Cytokines may be produced in and by peripheral nerve tissue during physiological and pathological processes by resident and recruited macrophages, mast cells, endothelial cells, and Schwann cells.

Why does histamine cause inflammation? ›

The message is, "Release histamines," which are stored in the mast cells. When they leave the mast cells, histamines boost blood flow in the area of your body the allergen affected. This causes inflammation, which lets other chemicals from your immune system step in to do repair work.

Why is histamine important? ›

Histamine is a signaling molecule, sending messages between cells. It tells stomach cells to make stomach acid. And it helps our brain stay awake.

Why does histamine increase? ›

The amount usually increases as the food ages, spoils, or ferments. Some foods and drinks also contain compounds that help release histamine in the body or block the production or effectiveness of the enzymes DAO and HNMT. Some foods and drinks that are rich in histamine include: alcohol.

What are primary mediators? ›

Primary mediators are subdivided further into preformed and newly synthesized mediators. Preformed mediators are formed and stored in the intracellular granules of mast cells and basophils. Newly synthesized mediators are derived from the metabolism of arachidonic acid, a phospholipid derived from cell membrane.

What are the immune mediators? ›

Cytokines are the mediators of the immune system. They are small proteins of around 25 kD that are produced in response to a stimulus (ie, invading microbes) by numerous cell types.

Is serotonin an inflammatory mediator? ›

The inflammatory mediators serotonin, prostaglandin E2 and bradykinin evoke calcium influx in rat sensory neurons. Neuroscience.


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