
n.
- The act of inflaming or the state of being inflamed.
- A localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss of function.
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American Heritage Dictionary:
in·flam·ma·tion |

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Britannica Concise Encyclopedia:
inflammation |
For more information on inflammation, visit Britannica.com.
McGraw-Hill Science & Technology Encyclopedia:
Inflammation |
The local response to injury, involving small blood vessels, the cells circulating within these vessels, and nearby connective tissue.
The early phases of the inflammatory response are stereotyped: A similar sequence of events occurs in a variety of tissue sites in response to a diversity of injuries. The response characteristically begins with hyperemia, edema, and adherence of the circulating white blood cells to endothelial cells. The white cells then migrate between the endothelial cells of the blood vessel into the tissue. The subsequent development of the inflammatory process is determined by factors such as type and location of injury, immune state of the host, and the use of therapeutic agents. See also Circulation; Edema.
A local inflammatory response is usually accompanied by systemic changes: fever, malaise, an increase in circulating leukocytes (leukocytosis), and increases in specific circulating proteins called acute-phase reactants. Such signals and symptoms are often helpful to the physician, first as clues to the presence of inflammation and later as an indication of its course.
The process of inflammation, both vascular and cellular, is orchestrated by an array of molecules produced locally. These mediators include histamine, leukotrienes, prostaglandins, complement components, kinins, antibodies, and interleukins. Many anti-inflammatory drugs function by preventing the formation of those mediators or by blocking their actions on the target cells whose behavior is modified by the mediators.
Inflammation is basically a protective mechanism. The leakage of water and protein into the injured area brings humoral factors, including antibodies, into the locale and may serve to dilute soluble toxic substances and wash them away. The adherence and migration of leukocytes brings them to the local site to deal with infectious agents. There are also instances in which no causative toxic substance or infectious agent can be found to account for the inflammation. This is the case in rheumatoid arthritis and rheumatic fever. Such diseases may be examples in which an uncontrolled or misdirected inflammatory response with an autoimmune component is turned against the host. See also Arthritis; Autoimmunity; Infection; Rheumatic fever.
Oxford Companion to the Body:
inflammation |
The word incorporates the Greek for flame, and indeed an inflamed body part may feel ‘on fire’. In its traditional clinical description, inflammation has four characteristics: calor (heat), rubor (redness), tumor (swelling and dolor (pain). They are the manifestations of the body's defence against injury or against invasion by foreign material or microorganisms, including the means of removal or destruction of the offending agent, restriction of the spread of infection, and preparations for the healing process. But the immune system that implements vital self-preservation may also sometimes cause inflammation by misdirected attack on some part of the body itself.
Inflammation can occur anywhere, acutely in the skin around a wound or a sting, or in less visible sites such as the lining of the middle ear, or of the bladder, or of the gall bladder. Chronically it can be related to persistent infection, ulceration, mechanical or chemical irritation, or autoimmune disease. Wherever inflammation occurs there are certain local mechanisms in common, despite differences in the precipitating factors and also in the relative prominence of the four cardinal features. Even with relatively minor and apparently localized problems, there are whole-body responses. Wherever inflammation is located, the condition is given a name ending in-itis, prefixed by the traditional name of the body part, such as arthritis for the joints, gastritis for the stomach, pericarditis for the membranes around the heart, ileitis for the small intestine, osteitis for bone, encephalitis for the brain.
Tissue damage results in the release by cells of various chemical agents, including prostaglandins. Vasodilator substances relax the blood vessels in their vicinity and the resulting increase in blood flow accounts for the redness and heat; swelling follows from increased permeability of blood vessels. This all enhances the supply of factors normally present in the blood that are important for the inflammatory response, including white blood cells and certain proteins in the plasma. Locally released substances (cytokines), as well as bacterial toxins if there is infection, attract cells of the immune system — macrophages and lymphocytes.
The nerves that carry the signals, set up by chemical and mechanical stimulation of sensory receptors, that we perceive as pain, themselves in turn promote an increase in local blood flow through the axon reflex mechanism. The nerve fibres (axons) give off branches back to their site of origin, and these release ‘substance P’, a peptide that relaxes the vessel walls. This, together with prostaglandins and other substances released from damaged tissues and also from the macrophages that congregate at the site, increases the sensitivity of sensory nerve endings, enhancing pain.
The events are not confined to the focus of trouble. Cytokines circulating in the blood provoke diverse whole-body responses. A major site of action is the hypothalamus, where they can affect its regulation of pituitary secretions, of sympathetic nervous system activity, and of body temperature. Whilst the resulting responses mainly promote the many aspects of defence, some also modify reactions that might otherwise be excessive: endorphin release modifies pain, and the increase in secretion of corticosteroids has anti-inflammatory effects, including toning down the activity of macrophages and interfering with prostaglandin synthesis.
The manifestations of inflammation vary greatly with the nature and severity of the insult and whether the process is rapidly or slowly developing. It can be simply serous, with fluid exudation, such as in a blister or a swollen joint, or in the rhinitis (of the nose) at the start of a common cold. With some types of infection it can be suppurative, where tissue and immune cell debris form a collection of pus; and chronic inflammation can be granulomatous, with nodules composed of packed inflammatory cells.
The phenomena of inflammation reflect an appropriate response to infection, or to mechanical damage either by acute injury or prolonged pressure or friction. When they occur inappropriately as a reaction against the body's own tissues the manifestations are similar. Thus conditions that might be called ‘inflammatory’ may refer to chronic infections, or to degenerative processes (as in osteoarthritis), or they may result from congenital abnormalities (as in cystic fibrosis) or autoimmune disease (such as rheumatoid arthritis or regional ileitis (Crohn's disease) ).
It would be inappropriate to attempt by treatment to diminish the body's responses, in terms of both local and widespread effects, if and when they were entirely appropriate and necessary to contain or cure the condition. Alleviation of the pain of inflammation by analgesic drugs is clearly beneficial to the sufferer; otherwise the first concern of treatment is if possible to remove the cause (such as treating infection by antibiotics, or removing foreign material). Other treatments in recent decades have been directed against inflammation itself, in conditions related to injury, ‘wear-and-tear’, and auto-immunity. Imitation and enhancement of the body's own anti-inflammatory corticosteroids became possible with synthetic steroid preparations, but there are undesirable side-effects. Along with the understanding of the role of prostaglandins in the mediation of inflammation and fever, a whole family of ‘non-steroidal antiflammatory drugs’ (NSAIDS) were developed, and they are widely used for a variety of muscle and joint problems, from accidental sprains to widespread arthritis. These drugs inhibit enzymes necessary for formation of prostaglandins, thus diminishing their local and general effects. (aspirin was well known to be useful in this context long before it was known to act by this mechanism.) No evidence has emerged for any positive or negative effect on the progress of the underlying conditions themselves (as opposed to relief of the symptoms), supporting the notion that the body's inflammatory responses are not always useful. Symptoms may indeed be relieved, but there are side-effects of NSAIDS, particularly gastrointestinal complications, related to the inhibition of prostaglandin synthesis where and when it is normally needed.
— Sheila Jennett
See also autoimmune diseases; fever; immune system; infection; infectious diseases; injury; pain; prostaglandins.
Roget's Thesaurus:
inflammation |
noun
Oxford Dictionary of Sports Science & Medicine:
inflammation |
non-specific defensive response of tissues to a physical or chemical injury, or bacterial infection. The response includes dilation (widening) of blood vessels and an increase in vessel permeability. It is indicated by redness, heat, swelling, pain, and dysfunction. Inflammation destroys, dilutes, or isolates the injurious agent and the injured tissue. Non-steroidal anti-inflammatories are often used to alleviate the symptoms and localize the inflammatory response. Some physical therapies (e.g. ultrasound) actually accelerate the inflammatory response, stimulating the activity of mast cells (large cells in connective tissue, which produce inflammatory chemicals) and accelerating the normal repair process. Chronic inflammatory conditions caused by overuse injuries can be self-perpetuating and require strong anti-inflammatories (e.g. steroid injections) to resolve them.
Columbia Encyclopedia:
inflammation |
Dictionary of Cultural Literacy: Health:
inflammation |
The response of tissue to injury or infection. Pain, heat, redness, and swelling are the four basic symptoms of inflammation.
Oxford Dictionary of Biochemistry:
inflammation |
| inflammable, infinitely thin, infinitely thick | |
| influenza virus, informatics, information |
Saunders Veterinary Dictionary:
inflammation |
A localized protective response elicited by injury or destruction of tissues, which serves to destroy, dilute, or wall off both the injurious agent and the injured tissue.
The inflammatory response can be provoked by physical, chemical and biological agents, including mechanical trauma, exposure to excessive amounts of sunlight, x-rays and radioactive materials, corrosive chemicals, extremes of heat and cold, and infectious agents such as bacteria, viruses and other pathogenic microorganisms. Although these infectious agents can produce inflammation, infection and inflammation are not synonymous.
The classic signs of inflammation are heat, redness, swelling, pain and loss of function. These are manifestations of the physiological changes that occur during the inflammatory process. The three major components of this process are: (1) changes in the caliber of blood vessels and the rate of blood flow through them (hemodynamic changes); (2) increased capillary permeability; and (3) leukocytic exudation.
Mosby's Dental Dictionary:
inflammation |
The cellular and vascular response or reaction to injury. Inflammation is characterized by pain, redness, swelling, heat, and disturbance of function. It may be acute or chronic. The term is not synonymous with infection, which implies an inflammatory reaction initiated by invasion of living organisms.
Random House Word Menu:
categories related to 'inflammation' |

Wikipedia on Answers.com:
Inflammation |
Inflammation (Latin, īnflammō, "I ignite, set alight") is part of the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.[1] Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process. 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.[2]
Without inflammation, wounds and infections would never heal. Similarly, progressive destruction of the tissue would compromise the survival of the organism. However, chronic inflammation can also lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). It is for that reason that inflammation is normally closely regulated by the body.
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 (especially granulocytes ) from the blood into the injured tissues. A cascade of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.
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Contents
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| Acute | Chronic | |
|---|---|---|
| Causative agent | Bacterial Pathogens, injured tissues | Persistent acute inflammation due to non-degradable pathogens,viral infection, persistent foreign bodies, or autoimmune reactions |
| Major cells involved | neutrophils (primarily), eosinophils and basophils (response to helminth worms and parasites), mononuclear cells (monocytes, macrophages) | Mononuclear cells (monocytes, macrophages, lymphocytes, plasma cells), fibroblasts |
| Primary mediators | Vasoactive amines, eicosanoids | IFN-γ and other cytokines, growth factors, reactive oxygen species, hydrolytic enzymes |
| Onset | Immediate | Delayed |
| Duration | Few days | Up to many months, or years |
| Outcomes | Resolution, abscess formation, chronic inflammation | Tissue destruction, fibrosis, necrosis |
| English | Latin | |
|---|---|---|
| Redness | Rubor* | |
| Swelling | Tumor* | |
| Heat | Calor* | |
| Pain | Dolor* | |
| Loss of function | Functio laesa** | |
| All the above signs may be observed in specific instances, but no single sign must, as a matter of course, be present.[3]
These are the original, or "cardinal signs" of inflammation.[3]* Functio laesa is an apocryphal notion, as it is not unique to inflammation and is a characteristic of many disease states.[4]** |
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Acute inflammation is a short-term process, usually appearing within a few minutes or hours and ceasing upon the removal of the injurious stimulus.[5] It is characterized by five cardinal signs:[6]
The acronym that may be used for this is "PRISH" for Pain, Redness, Immobility (loss of function), Swelling and Heat.
The traditional names for signs of inflammation come from Latin:
The first four (classical signs) were described by Celsus (ca 30 BC–38 AD),[8] while loss of function was added later by Galen[9] even though the attribution is disputed and the origination of the fifth sign has also been ascribed to Thomas Sydenham[10] and Virchow.[5][6]
Redness and heat are due to increased blood flow at body core temperature to the inflamed site; swelling is caused by accumulation of fluid; pain is due to release of chemicals that stimulate nerve endings. Loss of function has multiple causes.[6]
These five signs appear when acute inflammation occurs on the body's surface, whereas acute inflammation of internal organs may not result in the full set. Pain only happens where the appropriate sensory nerve endings exist in the inflamed area—e.g., acute inflammation of the lung (pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings.[6]
The process of acute inflammation is initiated by cells already present in all tissues, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells and mastocytes. These cells present on their surfaces certain receptors named pattern recognition receptors (PRRs), which recognize molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs). At the onset of an infection, burn, or other injuries, these cells undergo activation (one of their PRRs recognize a PAMP) and release inflammatory mediators responsible for the clinical signs of inflammation. Vasodilation and its resulting increased blood flow causes the redness (rubor) and increased heat (calor). Increased permeability of the blood vessels results in an exudation (leakage) of plasma proteins and fluid into the tissue (edema), which manifests itself as swelling (tumor). Some of the released mediators such as bradykinin increase the sensitivity to pain (hyperalgesia, dolor). The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly neutrophils, outside of the blood vessels (extravasation) into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury.[5] The loss of function (functio laesa) is probably the result of a neurological reflex in response to pain.
In addition to cell-derived mediators, several acellular biochemical cascade systems consisting of preformed plasma proteins act in parallel to initiate and propagate the inflammatory response. These include the complement system activated by bacteria, and the coagulation and fibrinolysis systems activated by necrosis, e.g. a burn or a trauma.[5]
The acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators have short half lives and are quickly degraded in the tissue. Hence, acute inflammation ceases once the stimulus has been removed.[5]
The exudative component involves the movement of plasma fluid, containing important proteins such as fibrin and immunoglobulins (antibodies), into inflamed tissue. This movement is achieved via the chemically induced dilation and increased permeability of blood vessels, which results in a net loss of blood plasma. The increased collection of fluid into the tissue causes it to swell (edema). This extravasated fluid is funneled by lymphatics to the regional lymph nodes, flushing bacteria along to start the recognition and attack phase of the adaptive immune system system.
Acute inflammation is characterised by marked vascular changes, including vasodilation, increased permeability and the slowing of blood flow, which are induced by the actions of various inflammatory mediators. Vasodilation occurs first at the arteriole level, progressing to the capillary level, and brings about a net increase in the amount of blood present, causing the redness and heat of inflammation. Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood - a condition characterized by enlarged vessels packed with cells. Stasis allows leukocytes to marginate (move) along the endothelium, a process critical to their recruitment into the tissues. Normal flowing blood prevents this, as the shearing force along the periphery of the vessels moves cells in the blood into the middle of the vessel.
* non-exhaustive list
| Name | Produced by | Description |
|---|---|---|
| Bradykinin | Kinin system | A vasoactive protein which is able to induce vasodilation, increase vascular permeability, cause smooth muscle contraction, and induce pain. |
| C3 | Complement system | Cleaves to produce C3a and C3b. C3a stimulates histamine release by mast cells, thereby producing vasodilation. C3b is able to bind to bacterial cell walls and act as an opsonin, which marks the invader as a target for phagocytosis. |
| C5a | Complement system | Stimulates histamine release by mast cells, thereby producing vasodilation. It is also able to act as a chemoattractant to direct cells via chemotaxis to the site of inflammation. |
| Factor XII (Hageman Factor) | Liver | A protein which circulates inactively, until activated by collagen, platelets, or exposed basement membranes via conformational change. When activated, it in turn is able to activate three plasma systems involved in inflammation: the kinin system, fibrinolysis system, and coagulation system. |
| Membrane attack complex | Complement system | A complex of the complement proteins C5b, C6, C7, C8, and multiple units of C9. The combination and activation of this range of complement proteins forms the membrane attack complex, which is able to insert into bacterial cell walls and causes cell lysis with ensuing death. |
| Plasmin | Fibrinolysis system | Able to break down fibrin clots, cleave complement protein C3, and activate Factor XII. |
| Thrombin | Coagulation system | Cleaves the soluble plasma protein fibrinogen to produce insoluble fibrin, which aggregates to form a blood clot. Thrombin can also bind to cells via the PAR1 receptor to trigger several other inflammatory responses, such as production of chemokines and nitric oxide. |
The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release enzymatic granules which damage pathogenic invaders. Leukocytes also release inflammatory mediators which develop and maintain the inflammatory response. Generally speaking, acute inflammation is mediated by granulocytes, while chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.
Various leukocytes are critically involved in the initiation and maintenance of inflammation. These cells must be able to get to the site of injury from their usual location in the blood, therefore mechanisms exist to recruit and direct leukocytes to the appropriate place. The process of leukocyte movement from the blood to the tissues through the blood vessels is known as extravasation, and can be divided up into a number of broad steps:
* non-exhaustive list
| Name | Type | Source | Description |
|---|---|---|---|
| Lysosome granules | Enzymes | Granulocytes | These cells contain a large variety of enzymes which perform a number of functions. Granules can be classified as either specific or azurophilic depending upon the contents, and are able to break down a number of substances, some of which may be plasma-derived proteins which allow these enzymes to act as inflammatory mediators. |
| Histamine | Vasoactive amine | Mast cells, basophils, platelets | Stored in preformed granules, histamine is released in response to a number of stimuli. It causes arteriole dilation and increased venous permeability. |
| IFN-γ | Cytokine | T-cells, NK cells | Antiviral, immunoregulatory, and anti-tumour properties. This interferon was originally called macrophage-activating factor, and is especially important in the maintenance of chronic inflammation. |
| IL-8 | Chemokine | Primarily macrophages | Activation and chemoattraction of neutrophils, with a weak effect on monocytes and eosinophils. |
| Leukotriene B4 | Eicosanoid | Leukocytes | Able to mediate leukocyte adhesion and activation, allowing them to bind to the endothelium and migrate across it. In neutrophils, it is also a potent chemoattractant, and is able to induce the formation of reactive oxygen species and the release of lysosome enzymes by these cells. |
| Nitric oxide | Soluble gas | Macrophages, endothelial cells, some neurons | Potent vasodilator, relaxes smooth muscle, reduces platelet aggregation, aids in leukocyte recruitment, direct antimicrobial activity in high concentrations. |
| Prostaglandins | Eicosanoid | Mast cells | A group of lipids which can cause vasodilation, fever, and pain. |
| TNF-α and IL-1 | Cytokines | Primarily macrophages | Both affect a wide variety of cells to induce many similar inflammatory reactions: fever, production of cytokines, endothelial gene regulation, chemotaxis, leukocyte adherence, activation of fibroblasts. Responsible for the systemic effects of inflammation, such as loss of appetite and increased heart rate. |
Specific patterns of acute and chronic inflammation are seen during particular situations that arise in the body, such as when inflammation occurs on an epithelial surface, or pyogenic bacteria are involved.
Inflammatory abnormalities are a large group of disorders which underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, demonstrated in both allergic reactions and some myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with etiological origins in inflammatory processes include cancer, atherosclerosis, and ischaemic heart disease.[5]
A large variety of proteins are involved in inflammation, and any one of them is open to a genetic mutation which impairs or otherwise dysregulates the normal function and expression of that protein.
Examples of disorders associated with inflammation include:
Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance. Clinical Cardiology: New Frontiers (Inflammation and Atherosclerosis)
An allergic reaction, formally known as type 1 hypersensitivity, is the result of an inappropriate immune response triggering inflammation. A common example is hay fever, which is caused by a hypersensitive response by skin mast cells to allergens. Pre-sensitised mast cells respond by degranulating, releasing vasoactive chemicals such as histamine. These chemicals propagate an excessive inflammatory response characterised by blood vessel dilation, production of pro-inflammatory molecules, cytokine release, and recruitment of leukocytes.[5] Severe inflammatory response may mature into a systemic response known as anaphylaxis.
Other hypersensitivity reactions (type 2 and type 3) are mediated by antibody reactions and induce inflammation by attracting leukocytes which damage surrounding tissue.[5]
Inflammatory myopathies are caused by the immune system inappropriately attacking components of muscle, leading to signs of muscle inflammation. They may occur in conjunction with other immune disorders, such as systemic sclerosis, and include dermatomyositis, polymyositis, and inclusion body myositis.[5]
Due to the central role of leukocytes in the development and propagation of inflammation, defects in leukocyte function often result in a decreased capacity for inflammatory defense with subsequent vulnerability to infection.[5] Dysfunctional leukocytes may be unable to correctly bind to blood vessels due to surface receptor mutations, digest bacteria (Chediak-Higashi syndrome), or produce microbicides (chronic granulomatous disease). Additionally, diseases affecting the bone marrow may result in abnormal or few leukocytes.
Certain drugs or exogenic chemical compounds are known to affect inflammation. Vitamin A deficiency causes an increase in inflammatory responses,[11] and anti-inflammatory drugs work specifically by inhibiting normal inflammatory components. Certain illicit drugs such as cocaine and ecstasy may exert some of their detrimental effects by activating transcription factors intimately involved with inflammation (e.g. NF-κB).[12][13]
Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration. Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis.[14] On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.
The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues.[5] Failure to do so results in chronic inflammation, and cellular destruction. Resolution of inflammation occurs by different mechanisms in different tissues. Mechanisms which serve to terminate inflammation include:[5][15]
| “ | Acute inflammation normally resolves by mechanisms that have remained somewhat elusive. Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins. After entering tissues, granulocytes promote the switch of arachidonic acid–derived prostaglandins and leukotrienes to lipoxins, which initiate the termination sequence. Neutrophil recruitment thus ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids, of resolvins and protectins, which critically shorten the period of neutrophil infiltration by initiating apoptosis. Consequently, apoptotic neutrophils undergo phagocytosis by macrophages, leading to neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming growth factor-β1. The anti-inflammatory program ends with the departure of macrophages through the lymphatics.[25] | ” |
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—Charles Serhan |
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An infectious organism can escape the confines of the immediate tissue via the circulatory system or lymphatic system, where it may spread to other parts of the body. If an organism is not contained by the actions of acute inflammation it may gain access to the lymphatic system via nearby lymph vessels. An infection of the lymph vessels is known as lymphangitis, and infection of a lymph node is known as lymphadenitis. A pathogen can gain access to the bloodstream through lymphatic drainage into the circulatory system.
When inflammation overwhelms the host, systemic inflammatory response syndrome is diagnosed. When it is due to infection, the term sepsis is applied, with the terms bacteremia being applied specifically for bacterial sepsis and viremia specifically to viral sepsis. Vasodilation and organ dysfunction are serious problems associated with widespread infection that may lead to septic shock and death.
Inflammation also induces high systemic levels of acute-phase proteins. In acute inflammation, these proteins prove beneficial, however in chronic inflammation they can contribute to amyloidosis.[5] These proteins include C-reactive protein, serum amyloid A, and serum amyloid P, which cause a range of systemic effects including[5]:
Inflammation often affects the numbers of leukocytes present in the body:
With the discovery of interleukins (IL), the concept of systemic inflammation developed. Although the processes involved are identical to tissue inflammation, systemic inflammation is not confined to a particular tissue but involves the endothelium and other organ systems.
Chronic inflammation is widely observed in obesity.[26] The obese commonly have many elevated markers of inflammation, including[27][28]:
Low-grade chronic inflammation is characterized by a two- to threefold increase in the systemic concentrations of cytokines such as TNF-α, IL-6, and CRP.[31] Waist circumference correlates significantly with systemic inflammatory response.[32] A predominant factor in this correlation is due to the autoimmune response triggered by adiposity, whereby immune cells may mistake fatty deposits for intruders. The body attacks fat similar to bacteria and fungi. When expanded fat cells leak or break open, macrophages mobilize to clean up and embed into the adipose tissue. Then macrophages release inflammatory chemicals, including TNF-α and (IL-6). TNF's primary role is to regulate the immune cells and induce inflammation. White blood cells then assist by releasing more cytokines. This link between adiposity and inflammation has been shown to produce 10-35% of IL-6 in a resting individual, and this production increases with increasing adiposity.[33]
During clinical studies, inflammatory-related molecule levels were reduced and increased levels of anti-inflammatory molecules were seen within four weeks after patients began a very low calorie diet.[34] The association of systemic inflammation with insulin resistance and atherosclerosis is the subject of intense research.[35]
Inflammation and macrophage-specific genes are unregulated in white adipose tissue (WAT). There were also signs of dramatic increase in circulating insulin level, adipocyte lipolysis and formation of multinucleate giant cells. The fat-derived protein called angiopoietin-like protein 2 (Angptl2) elevates in fat tissues. Higher than normal Angptl2 level in fat tissues develop inflammation as well as insulin and leptin resistance. Stored fat secretes Leptin to signal satiety. Leptin resistance plays a role in the process where appetite overrules the message of satiety. Angptl2 then starts an inflammatory cascade causing blood vessels to remodel and attract macrophages. Angptl2 is an adipocyte-derived inflammatory mediator linking obesity to systemic insulin resistance.[citation needed] It is possible that, as an inflammatory marker, leptin responds specifically to adipose-derived inflammatory cytokines.
C-reactive protein (CRP) is generated at a higher level in obese people. It raises when there is inflammation throughout the body. Mild elevation in CRP increase risk of heart attacks, strokes, high blood pressure, muscle weakness and fragility.[citation needed]
Hyperglycemia induces IL-6 production from endothelial cells and macrophages.[36] Meals high in saturated fat, as well as meals high in calories have been associated with increases in inflammatory markers.[37][38] While the inflammatory responses are acute and arise in response to overeating, the response may become chronic if the overeating is chronic.
The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent that is causing it. Here are the possible outcomes to inflammation:[5]
Inflammation is usually indicated by adding the suffix "-itis", as shown below. However, some conditions such as asthma and pneumonia do not follow this convention. More examples are available at list of types of inflammation.
Acute appendicitis
Acute dermatitis
Acute infective meningitis
Acute tonsillitis
Acute inflammation of the muscle cells, as understood in exercise physiology,[39] can result after induced eccentric and concentric muscle training. Participation in eccentric training and conditioning, including resistance training and activities that emphasize eccentric lengthening of the muscle including downhill running on a moderate to high incline can result in considerable soreness within 24 to 48 hours, even though blood lactate levels, previously thought to cause muscle soreness, were much higher with level running. This delayed onset muscle soreness (DOMS) results from structural damage to the contractile filaments and z-disks, which has been noted especially in marathon runners whose muscle fibers revealed remarkable damage to the muscle fibers after both training and marathon competition. The onset and timing of this gradient damage to the muscle parallels the degree of muscle soreness experienced by the runners.
Z-disks are the point of contact for the contractile proteins. They provide structural support for the transmission of force when the muscle fibers are activated to shorten. However, in marathon runners and those who prescribe to the overload principle to enhance their muscles, show moderate Z-disk streaming and major disruption of the thick and thin filaments in parallel groups of sarcomeres as a result of the force of eccentric actions or stretching of the tightened muscle fibers.
This disruption of the muscle fibers triggers white blood cells to increase following the induced muscle soreness, leading to the inflammatory response observation from the induced muscle soreness. Elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure are concluded to be associated with the inflammatory response. High tension in the contractile-elastic system of muscle results in structural damage to the muscle fiber and plasmalemma and its epimysium, perimysium, and/or endomysium. The mysium damage disrupts calcium homeostasis in the injured fiber and fiber bundles, resulting in necrosis that peaks about 48 hours after exercise. The products of the macrophage activity and intracellular contents (such as histamines, kinins, and K+) accumulate outside the cells. These substances then stimulate the free nerve endings in the muscle; a process that appears accentuated by eccentric exercise, in which large forces are distributed over relatively small cross-sectional area of the muscle.
There is a known relationship between inflammation and muscle growth.[40] For instance, high doses of anti-inflammatory medicines (e.g., NSAIDs) are able to blunt muscle growth.[41][42]
It has been further theorized that the acute localized inflammatory responses to muscular contraction during exercise, as described above, are a necessary precursor to muscle growth.[43] As a response to muscular contractions, the acute inflammatory response initiates the breakdown and removal of damaged muscle tissue.[44] Muscles can synthesize cytokines in response to contractions,[45][46][47] such that the cytokines Interleukin-1 beta (IL-1β), TNF-α, and IL-6 are expressed in skeletal muscle up to 5 days after exercise.[44]
In particular, the increase in levels of IL-6 can reach up to one hundred times that of resting levels.[47] Depending on volume, intensity, and other training factors, the IL-6 increase associated with training initiates about 4 hours after resistance training and remains elevated for up to 24 hours.[48][49][50]
These acute increases in cytokines, as a response to muscle contractions, help initiate the process of muscle repair and growth by activating satellite cells within the inflamed muscle. Satellite cells are crucial for skeletal muscle adaption to exercise.[51] They contribute to hypertrophy by providing new myonuclei and repair damaged segments of mature myofibers for successful regeneration following injury- or exercise-induced muscle damage;[52][53][54] high-level powerlifters can have up to 100% more satellite cells than untrained controls.[55][56]
A rapid and transient localization of the IL-6 receptor and increased IL-6 expression occurs in satellite cells following contractions.[48] IL-6 has been shown to mediate hypertrophic muscle growth both in vitro and in vivo.[51] Unaccustomed exercise can increase IL-6 by up to sixfold at 5 hours post-exercise and threefold 8 days after exercise.[57] Also telling is the fact that NSAIDs can decrease satellite cell response to exercise,[41] thereby reducing exercise-induced protein synthesis.[42]
The increase in cytokines after resistance exercise coincides with the decrease in levels of myostatin, a protein that inhibits muscle differentiation and growth.[50] The cytokine response to resistance exercise and moderate-intensity running occur differently, with the latter causing a more prolonged response, especially at the 12-24 hour mark.[50]
Both chronic and extreme inflammation are associated with disruptions of anabolic signals initiating muscle growth. Chronic inflammation has been implicated as part of the cause of the muscle loss that occurs with aging.[40][58] Increased protein levels of myostatin have been described in patients with diseases characterized by chronic low-grade inflammation.[59] Increased levels of TNF-α can suppress the AKT/mTOR pathway, a crucial pathway for regulating skeletal muscle hypertrophy,[60] thereby increasing muscle catabolism.[61][62][63] Cytokines may antagonize the anabolic effects of Insulin-like growth factor 1 (IGF-1).[64][65] In the case of sepsis, an extreme whole body inflammatory state, the synthesis of both myofibrillar and sarcoplasmic proteins are inhibited, with the inhibition taking place preferentially in fast-twitch muscle fibers.[64][66] Sepsis is also able to prevent leucine from stimulating muscle protein synthesis.[45] In animal models, when inflammation is created, mTOR loses its ability to be stimulated by muscle growth.[67]
Regular physical activity is reported to decrease markers of inflammation[quantify],[68][69][70] although the correlation is imperfect and seems to reveal differing results contingent upon training intensity. For instance, while baseline measurements of circulating inflammatory markers do not seem to differ greatly between healthy trained and untrained adults,[71][72] long-term chronic training may help reduce chronic low-grade inflammation.[73] On the other hand, levels of inflammatory markers (IL-6) remained elevated longer into the recovery period following an acute bout of exercise in patients with inflammatory diseases, relative to the recovery of healthy controls.[73] It may well be that low-intensity training can reduce resting pro-inflammatory markers (CRP, IL-6), while moderate-intensity training has milder and less-established anti-inflammatory benefits.[71][74][75][76] There is a strong relationship between exhaustive exercise and chronic low-grade inflammation.[77] Marathon running may enhance IL-6 levels as much as 100 times over normal and increases total leuckocyte count and neturophil mobilization.[77] As such, individuals pursuing exercise as a means to treat the other factors behind chronic inflammation may wish to balance their exercise protocol with bouts of low-intensity training, while striving to avoid chronic over-exertion.
Given that localized acute inflammation is a necessary component for muscle growth, and that chronic low-grade inflammation is associated with a disruption of anabolic signals initiating muscle growth, it has been theorized that a signal-to-noise model may best describe the relationship between inflammation and muscle growth.[78] By keeping the "noise" of chronic inflammation to a minimum, the localized acute inflammatory response signals a stronger anabolic response than could be achieved with higher levels of chronic inflammation.
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Translations:
Inflammation |
Dansk (Danish)
n. - antændelse, betændelse, inflammation
idioms:
Nederlands (Dutch)
ontsteking, ontbranding
Français (French)
n. - (Méd) inflammation, inflammation (d'un combustible), (fig) excitation
Deutsch (German)
n. - Entzündung, Aufflammen, Aufstacheln
Ελληνική (Greek)
n. - (ιατρ.) φλεγμονή, (μτφ.) έξαψη, παροξυσμός, ερεθισμός
idioms:
Italiano (Italian)
combustione, infiammazione
Português (Portuguese)
n. - inflamação (f)
Русский (Russian)
воспламенение, воспаление
Español (Spanish)
n. - combustión, inflamación
Svenska (Swedish)
n. - inflammation, upphetsning, antändning
中文(简体)(Chinese (Simplified))
怒火, 燃烧, 发火
idioms:
中文(繁體)(Chinese (Traditional))
n. - 怒火, 燃燒, 發火
idioms:
한국어 (Korean)
n. - 점화, 연소, 염증 , 격노
日本語 (Japanese)
n. - 点火, 燃焼, 燃え上がり, 炎症, 発火
idioms:
العربيه (Arabic)
(الاسم) التهاب, اشتعال
עברית (Hebrew)
n. - דלקת, הדלקה, שלהוב
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