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autoimmune disorder

Inflammation (from

cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

The five


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

mononuclear cells, and is characterized by simultaneous destruction and healing
of the tissue from the inflammatory process.

Inflammation has also been classified as Type 1 and Type 2 based on the type of

helper T cells (Th1 and Th2) involved.[4]

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

autoimmune diseases (including type III hypersensitivity







Comparison between acute and chronic inflammation:
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), basophils (inflammatory response), and eosinophils (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


Acute inflammation occurs immediately upon injury, lasting only a few days.[8] Cytokines and chemokines promote the migration of neutrophils and macrophages to the site of inflammation.[8] Pathogens, allergens, toxins, burns, and frostbite are some of the typical causes of acute inflammation.[8] Toll-like receptors (TLRs) recognize microbial pathogens.[8] Acute inflammation can be a defensive mechanism to protect tissues against injury.[8] Inflammation lasting 2–6 weeks is designated subacute inflammation.[8][9]

Cardinal signs

The classic signs and symptoms of acute inflammation:[a]
English Latin
Heat Calor
Pain Dolor
Loss of function Functio laesa[b]

Acute inflammation is a short-term process, usually appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus.

cardinal signs:[14]

The traditional names for signs of inflammation come from Latin:

The first four (classical signs) were described by


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 the release of chemicals such as bradykinin and histamine that stimulate nerve endings. Loss of function has multiple causes.[14]

Acute inflammation of the lung (usually as in response to

parietal pleura, which does have pain-sensitive nerve endings.[14]

Acute process

A flowchart depicting the events of acute inflammation.[19]
Micrograph showing granulation tissue. H&E stain

The process of acute inflammation is initiated by resident immune cells already present in the involved tissue, mainly resident

Kupffer cells and mast cells. These cells possess surface receptors known as pattern recognition receptors (PRRs), which recognize (i.e., bind) two subclasses of molecules: pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). PAMPs are compounds that are associated with various pathogens
, but which are distinguishable from host molecules. DAMPs are compounds that are associated with host-related injury and cell damage.

At the onset of an infection, burn, or other injuries, these cells undergo activation (one of the PRRs recognize a PAMP or DAMP) 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

chemotactic gradient created by the local cells to reach the site of injury.[12]
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

fibrinolysis systems activated by necrosis (e.g., burn, trauma).[12]

Acute inflammation may be regarded as the first line of defense against injury. Acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the stimulus has been removed.[12]


Chronic inflammation is inflammation that lasts for months or years.

plasma cells predominate in chronic inflammation, in contrast to the neutrophils that predominate in acute inflammation.[9] Diabetes, cardiovascular disease, allergies, and chronic obstructive pulmonary disease (COPD) are examples of diseases mediated by chronic inflammation.[9] Obesity, smoking, stress and insufficient diet are some of the factors that promote chronic inflammation.[9] A 2014 study reported that 60% of Americans had at least one chronic inflammatory condition, and 42% had more than one.[9]

Cardinal signs

Common signs and symptoms that develop during chronic inflammation are:[9]

  • Body pain, arthralgia, myalgia
  • Chronic fatigue and insomnia
  • Depression, anxiety and mood disorders
  • Gastrointestinal complications such as constipation, diarrhea, and acid reflux
  • Weight gain or loss
  • Frequent infections

Vascular component

Vasodilation and increased permeability

As defined, acute inflammation is an immunovascular response to inflammatory stimuli, which can include infection or trauma.

), into inflamed tissue.

Upon contact with PAMPs, tissue

lymphatics to the regional lymph nodes, flushing bacteria along to start the recognition and attack phase of the adaptive immune system

ingrown toenail
showing the characteristic redness and swelling associated with acute inflammation

Acute inflammation is characterized by marked vascular changes, including

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.

Plasma cascade systems

  • The
  • The
    kinin system
    generates proteins capable of sustaining vasodilation and other physical inflammatory effects.
  • The
    coagulation system
    or clotting cascade, which forms a protective protein mesh over sites of injury.
  • The
    fibrinolysis system
    , which acts in opposition to the coagulation system, to counterbalance clotting and generate several other inflammatory mediators.

Plasma-derived mediators

* non-exhaustive list

Name Produced by Description
Kinin system
A vasoactive protein that is able to induce vasodilation, increase vascular permeability, cause smooth muscle contraction, and induce pain.
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
to direct cells via chemotaxis to the site of inflammation.
Factor XII (Hageman Factor) Liver A protein that 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 bacterial death.
Fibrinolysis system
Able to break down fibrin clots, cleave complement protein C3, and activate Factor XII.
Coagulation system
Cleaves the soluble plasma protein
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

Cellular component

The cellular component involves

leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation.[20] Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release enzymatic granules that damage pathogenic invaders. Leukocytes also release inflammatory mediators that develop and maintain the inflammatory response. In general, acute inflammation is mediated by granulocytes, whereas chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes

Leukocyte extravasation


, particularly neutrophils, are critically involved in the initiation and maintenance of inflammation. These cells must be able to move 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 broadly divided up into a number of steps:

  1. Leukocyte margination and endothelial adhesion: The white blood cells within the vessels which are generally centrally located move peripherally towards the walls of the vessels.
    G protein-coupled receptors
    that activates integrins on the leukocyte surface for firm adhesion. Such activation increases the affinity of bound integrin receptors for ICAM-1 and VCAM-1 on the endothelial cell surface, firmly binding the leukocytes to the endothelium.
  2. Migration across the endothelium, known as transmigration, via the process of
    diapedesis: Chemokine gradients stimulate the adhered leukocytes to move between adjacent endothelial cells. The endothelial cells retract and the leukocytes pass through the basement membrane into the surrounding tissue using adhesion molecules such as ICAM-1.[25]
  3. Movement of leukocytes within the tissue via
    , for example, C3a or C5, and cause the leukocytes to move along a chemotactic gradient towards the source of inflammation.


Extravasated neutrophils in the cellular phase come into contact with microbes at the inflamed tissue.

peptidoglycans, and surface proteins. Endocytic PRRs on phagocytes reflect these molecular patterns, with C-type lectin receptors binding to mannans and β-glucans, and scavenger receptors
binding to LPS.

Upon endocytic PRR binding,

bleach within the phagolysosomes then kill microbes inside the phagocyte.

Phagocytic efficacy can be enhanced by

elimination of the infective agent.

Cell-derived mediators

* non-exhaustive list

Name Type Source Description
Lysosome granules Enzymes Granulocytes These cells contain a large variety of enzymes that perform a number of functions. Granules can be classified as either
depending upon the contents, and are able to break down a number of substances, some of which may be plasma-derived proteins that allow these enzymes to act as inflammatory mediators.
GM-CSF Glycoprotein Macrophages, monocytes, T-cells, B-cells, and tissue-resident cells Elevated GM-CSF has been shown to contribute to inflammation in
Mast cells and basophils Stored in preformed granules, histamine is released in response to a number of stimuli. It causes
permeability, and a wide variety of organ-specific effects.
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-6 Cytokine and Myokine Macrophages, osteoblasts, adipocytes, and smooth muscle cells (cytokine) Skeletal muscle cells (myokine) Pro-inflammatory cytokine secreted by macrophages in response to pathogen-associated molecular patterns (PAMPs); pro-inflammatory cytokine secreted by adipocytes, especially in obesity; anti-inflammatory myokine secreted by skeletal muscle cells in response to exercise.
IL-8 Chemokine Primarily macrophages Activation and chemoattraction of neutrophils, with a weak effect on monocytes and eosinophils.
Leukotriene B4 Eicosanoid
, cancer cells
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 lysosomal enzymes by these cells.
These three Cysteine-containing leukotrienes contract lung airways, increase micro-vascular permeability, stimulate mucus secretion, and promote eosinophil-based inflammation in the lung, skin, nose, eye, and other tissues.
5-oxo-eicosatetraenoic acid
, cancer cells
Potent stimulator of neutrophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation; monocyte chemotaxis; and with even greater potency eosinophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation.
Metabolic precursor to 5-Oxo-eicosatetraenoic acid, it is a less potent stimulator of neutrophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation; monocyte chemotaxis; and eosinophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation.
Prostaglandins Eicosanoid Mast cells A group of lipids that can cause vasodilation, fever, and pain.
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.
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. TNF-α inhibits osteoblast differentiation.
Tryptase Enzymes Mast Cells This serine protease is believed to be exclusively stored in mast cells and secreted, along with histamine, during mast cell activation.[26][27][28]

Morphologic patterns

Specific patterns of acute and chronic inflammation are seen during particular situations that arise in the body, such as when inflammation occurs on an

bacteria are involved.


Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, as demonstrated in both

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 atherosclerosis from initiation through progression and, ultimately, the thrombotic complications from it. 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, the anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights on inflammation contribute to the etiology of atherosclerosis, and the practical clinical applications in risk stratification and the targeting of therapy for atherosclerosis.[29]


An allergic reaction, formally known as

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.[12] Severe inflammatory response may mature into a systemic response known as anaphylaxis


Leukocyte defects

Due to the central role of leukocytes in the development and propagation of inflammation, defects in leukocyte functionality often result in a decreased capacity for inflammatory defense with subsequent vulnerability to infection.

microbicides (chronic granulomatous disease). In addition, diseases affecting the bone marrow
may result in abnormal or few leukocytes.


Certain drugs or exogenous chemical compounds are known to affect inflammation.

ecstasy may exert some of their detrimental effects by activating transcription factors intimately involved with inflammation (e.g. NF-κB).[31][32]


Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration.

chemokines and their receptors for invasion, migration and metastasis.[34] On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.[35]
Molecular intersection between receptors of steroid hormones, which have important effects on cellular development, and transcription factors that play key roles in inflammation, such as NF-κB, may mediate some of the most critical effects of inflammatory stimuli on cancer cells.[36] This capacity of a mediator of inflammation to influence the effects of steroid hormones in cells is very likely to affect carcinogenesis. On the other hand, due to the modular nature of many steroid hormone receptors, this interaction may offer ways to interfere with cancer progression, through targeting of a specific protein domain in a specific cell type. Such an approach may limit side effects that are unrelated to the tumor of interest, and may help preserve vital homeostatic functions and developmental processes in the organism.

According to a review of 2009, recent data suggests that cancer-related inflammation (CRI) may lead to accumulation of random genetic alterations in cancer cells.[37]

Role in cancer

In 1863, Rudolf Virchow hypothesized that the origin of cancer was at sites of chronic inflammation.[34][38] At present, chronic inflammation is estimated to contribute to approximately 15% to 25% of human cancers.[38][39]

Mediators and DNA damage in cancer

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

TNF-α, IL-6 and IL-15 and chemokines such as IL-8 and GRO-alpha.[41][38] These inflammatory mediators, and others, orchestrate an environment that fosters proliferation and survival.[34][41]

Inflammation also causes DNA damages due to the induction of reactive oxygen species (ROS) by various intracellular inflammatory mediators.[34][41][38] In addition, leukocytes and other phagocytic cells attracted to the site of inflammation induce DNA damages in proliferating cells through their generation of ROS and reactive nitrogen species (RNS). ROS and RNS are normally produced by these cells to fight infection.[34] ROS, alone, cause more than 20 types of DNA damage.[42] Oxidative DNA damages cause both mutations[43] and epigenetic alterations.[44][38][45] RNS also cause mutagenic DNA damages.[46]

A normal cell may undergo carcinogenesis to become a cancer cell if it is frequently subjected to DNA damage during long periods of chronic inflammation. DNA damages may cause genetic mutations due to inaccurate repair. In addition, mistakes in the DNA repair process may cause epigenetic alterations.[38][41][45] Mutations and epigenetic alterations that are replicated and provide a selective advantage during somatic cell proliferation may be carcinogenic.

Genome-wide analyses of human cancer tissues reveal that a single typical cancer cell may possess roughly 100 mutations in coding regions, 10-20 of which are "driver mutations" that contribute to cancer development.[38] However, chronic inflammation also causes epigenetic changes such as DNA methylations, that are often more common than mutations. Typically, several hundreds to thousands of genes are methylated in a cancer cell (see DNA methylation in cancer). Sites of oxidative damage in chromatin can recruit complexes that contain DNA methyltransferases (DNMTs), a histone deacetylase (SIRT1), and a histone methyltransferase (EZH2), and thus induce DNA methylation.[38][47][48] DNA methylation of a CpG island in a promoter region may cause silencing of its downstream gene (see CpG site and regulation of transcription in cancer). DNA repair genes, in particular, are frequently inactivated by methylation in various cancers (see hypermethylation of DNA repair genes in cancer). A 2018 report[49] evaluated the relative importance of mutations and epigenetic alterations in progression to two different types of cancer. This report showed that epigenetic alterations were much more important than mutations in generating gastric cancers (associated with inflammation).[50] However, mutations and epigenetic alterations were of roughly equal importance in generating esophageal squamous cell cancers (associated with tobacco chemicals and acetaldehyde, a product of alcohol metabolism).


It has long been recognized that infection with HIV is characterized not only by development of profound

effective antiretroviral therapy (ART) and effective suppression of viremia in HIV-infected individuals, chronic inflammation persists. Animal studies also support the relationship between immune activation and progressive cellular immune deficiency: SIVsm infection of its natural nonhuman primate hosts, the sooty mangabey, causes high-level viral replication but limited evidence of disease.[56][57] This lack of pathogenicity is accompanied by a lack of inflammation, immune activation and cellular proliferation. In sharp contrast, experimental SIVsm infection of rhesus macaque produces immune activation and AIDS-like disease with many parallels to human HIV infection.[58]

Delineating how CD4 T cells are depleted and how chronic inflammation and immune activation are induced lies at the heart of understanding HIV pathogenesis––one of the top priorities for HIV research by the Office of AIDS Research, National Institutes of Health. Recent studies demonstrated that caspase-1-mediated pyroptosis, a highly inflammatory form of programmed cell death, drives CD4 T-cell depletion and inflammation by HIV.[59][60][61] These are the two signature events that propel HIV disease progression to AIDS. Pyroptosis appears to create a pathogenic vicious cycle in which dying CD4 T cells and other immune cells (including macrophages and neutrophils) release inflammatory signals that recruit more cells into the infected lymphoid tissues to die. The feed-forward nature of this inflammatory response produces chronic inflammation and tissue injury.[62] Identifying pyroptosis as the predominant mechanism that causes CD4 T-cell depletion and chronic inflammation, provides novel therapeutic opportunities, namely caspase-1 which controls the pyroptotic pathway. In this regard, pyroptosis of CD4 T cells and secretion of pro-inflammatory cytokines such as IL-1β and IL-18 can be blocked in HIV-infected human lymphoid tissues by addition of the caspase-1 inhibitor VX-765,[59] which has already proven to be safe and well tolerated in phase II human clinical trials.[63] These findings could propel development of an entirely new class of "anti-AIDS" therapies that act by targeting the host rather than the virus. Such agents would almost certainly be used in combination with ART. By promoting "tolerance" of the virus instead of suppressing its replication, VX-765 or related drugs may mimic the evolutionary solutions occurring in multiple monkey hosts (e.g. the sooty mangabey) infected with species-specific lentiviruses that have led to a lack of disease, no decline in CD4 T-cell counts, and no chronic inflammation.


The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues.[12] Failure to do so results in chronic inflammation, and cellular destruction. Resolution of inflammation occurs by different mechanisms in different tissues. Mechanisms that serve to terminate inflammation include:[12][64]

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,

cytokines such as transforming growth factor-β1. The anti-inflammatory program ends with the departure of macrophages through the lymphatics.[75]

Connection to depression

There is evidence for a link between inflammation and depression.[76] Inflammatory processes can be triggered by negative cognitions or their consequences, such as stress, violence, or deprivation. Thus, negative cognitions can cause inflammation that can, in turn, lead to depression.[77][78][dubious ] In addition, there is increasing evidence that inflammation can cause depression because of the increase of cytokines, setting the brain into a "sickness mode".[79] Classical symptoms of being physically sick, such as lethargy, show a large overlap in behaviors that characterize depression. Levels of cytokines tend to increase sharply during the depressive episodes of people with bipolar disorder and drop off during remission.[80] Furthermore, it has been shown in clinical trials that anti-inflammatory medicines taken in addition to antidepressants not only significantly improves symptoms but also increases the proportion of subjects positively responding to treatment.[81] Inflammations that lead to serious depression could be caused by common infections such as those caused by a virus, bacteria or even parasites.[82]

Connection to delirium

There is evidence for a link between inflammation and delirium based on the results of a recent longitudinal study investigating CRP in COVID-19 patients.[83]

Systemic effects


. When lymph nodes cannot destroy all pathogens, the infection spreads further. A pathogen can gain access to the bloodstream through lymphatic drainage into the circulatory system.

When inflammation overwhelms the host,

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.[84]

Acute-phase proteins

Inflammation also is characterized by high systemic levels of

serum amyloid P, which cause a range of systemic effects including:[12]

Leukocyte numbers

Inflammation often affects the numbers of leukocytes present in the body:

Interleukins and obesity

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.[85][86] Obese people commonly have many elevated markers of inflammation, including:[87][88]

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.[91] Waist circumference correlates significantly with systemic inflammatory response.[92]

Loss of white adipose tissue reduces levels of inflammation markers.[85] As of 2017 the association of systemic inflammation with insulin resistance and type 2 diabetes, and with atherosclerosis was under preliminary research, although rigorous clinical trials had not been conducted to confirm such relationships.[93]

cardiovascular diseases.[94]


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:[12]

  1. Resolution
    The complete restoration of the inflamed tissue back to a normal status. Inflammatory measures such as vasodilation, chemical production, and leukocyte infiltration cease, and damaged parenchymal cells regenerate. Such is usually the outcome when limited or short-lived inflammation has occurred.
  2. scarring occurs in these areas of damage, forming a scar composed primarily of collagen. The scar will not contain any specialized structures, such as parenchymal
    cells, hence functional impairment may occur.
  3. Abscess formation
    A cavity is formed containing pus, an opaque liquid containing dead white blood cells and bacteria with general debris from destroyed cells.
  4. Chronic inflammation
    In acute inflammation, if the injurious agent persists then chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a
    chronic wound. Chronic inflammation is characterised by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release—including reactive oxygen species—are injurious to the organism's own tissues as well as invading agents. As a consequence, chronic inflammation is almost always accompanied by tissue destruction.


Inflammation is usually indicated by adding the suffix "

List of types of inflammation

See also


  1. ^ All these signs may be observed in specific instances, but no single sign must, as a matter of course, be present.[10] These are the original, or
    cardinal signs of inflammation.[10]
  2. ^ Functio laesa is an antiquated notion, as it is not unique to inflammation and is a characteristic of many disease states.[11]


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  3. .
  4. .
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  11. PMID 5276838
  12. ^ .
  13. .
  14. ^ . Retrieved 5 November 2008.
  15. .
  16. .
  17. .
  18. .
  19. ^ Robbins S, Cotran R, Kumar V, Abbas A, Aster J (2020). Pathologic basis of disease (10th ed.). Philadelphia, PA: Saunders Elsevier.
  20. ^
    PMID 25833893
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  51. ^ .
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  63. ^ "Study of VX-765 in Subjects With Treatment-resistant Partial Epilepsy - Full Text View -". 19 December 2013. Retrieved 21 May 2016.
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  79. ^ Williams C (4 January 2015). "Is depression a kind of allergic reaction?". The Guardian.
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External links