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SpecialtyInflammation_header_cell_0_1_0 Immunology RheumatologyInflammation_cell_0_1_1
SymptomsInflammation_header_cell_0_2_0 Heat, pain, redness, swellingInflammation_cell_0_2_1
ComplicationsInflammation_header_cell_0_3_0 Asthma, pneumonia, autoimmune diseasesInflammation_cell_0_3_1
DurationInflammation_header_cell_0_4_0 acute Few days chronic Up to many months, or yearsInflammation_cell_0_4_1
CausesInflammation_header_cell_0_5_0 Bacteria, virusInflammation_cell_0_5_1

Inflammation (from Latin: ) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. Inflammation_sentence_0

The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair. Inflammation_sentence_1

The five classical signs of inflammation are heat, pain, redness, swelling, and loss of function (Latin calor, dolor, rubor, tumor, and functio laesa). Inflammation_sentence_2

Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen. Inflammation_sentence_3

Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. Inflammation_sentence_4

In contrast, chronic inflammation is associated with various diseases, such as hay fever, periodontal disease, atherosclerosis, and osteoarthritis. Inflammation_sentence_5

Inflammation can be classified as either acute or chronic. Inflammation_sentence_6

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. Inflammation_sentence_7

A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Inflammation_sentence_8

Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Inflammation_sentence_9

Inflammation is not a synonym for infection. Inflammation_sentence_10

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_sentence_11

Inflammation, on the other hand, describes purely the body's immunovascular response, whatever the cause may be. Inflammation_sentence_12

But because of how often the two are correlated, words ending in the suffix (which refers to inflammation) are sometimes informally described as referring to infection. Inflammation_sentence_13

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. Inflammation_sentence_14

It is useful to differentiate inflammation and infection because there are typical situations in pathology and medical diagnosis where inflammation is not driven by microbial invasion – for example, atherosclerosis, trauma, ischemia, and autoimmune diseases including type III hypersensitivity. Inflammation_sentence_15

Causes Inflammation_section_0

Types Inflammation_section_1

See also: List of types of inflammation by location Inflammation_sentence_16


Comparison between acute and chronic inflammation:Inflammation_table_caption_1
Inflammation_header_cell_1_0_0 AcuteInflammation_header_cell_1_0_1 ChronicInflammation_header_cell_1_0_2
Causative agentInflammation_cell_1_1_0 Bacterial pathogens, injured tissuesInflammation_cell_1_1_1 Persistent acute inflammation due to non-degradable pathogens, viral infection, persistent foreign bodies, or autoimmune reactionsInflammation_cell_1_1_2
Major cells involvedInflammation_cell_1_2_0 neutrophils (primarily), basophils (inflammatory response), and eosinophils (response to helminth worms and parasites), mononuclear cells (monocytes, macrophages)Inflammation_cell_1_2_1 Mononuclear cells (monocytes, macrophages, lymphocytes, plasma cells), fibroblastsInflammation_cell_1_2_2
Primary mediatorsInflammation_cell_1_3_0 Vasoactive amines, eicosanoidsInflammation_cell_1_3_1 IFN-γ and other cytokines, growth factors, reactive oxygen species, hydrolytic enzymesInflammation_cell_1_3_2
OnsetInflammation_cell_1_4_0 ImmediateInflammation_cell_1_4_1 DelayedInflammation_cell_1_4_2
DurationInflammation_cell_1_5_0 Few daysInflammation_cell_1_5_1 Up to many months, or yearsInflammation_cell_1_5_2
OutcomesInflammation_cell_1_6_0 Resolution, abscess formation, chronic inflammationInflammation_cell_1_6_1 Tissue destruction, fibrosis, necrosisInflammation_cell_1_6_2

Cardinal signs Inflammation_section_2

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. Inflammation_sentence_17

It involves a coordinated and systemic mobilization response locally of various immune, endocrine and neurological mediators of acute inflammation. Inflammation_sentence_18

In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and then ceases. Inflammation_sentence_19

It is characterized by five cardinal signs: Inflammation_sentence_20

An acronym that may be used to remember the key symptoms is "PRISH", for pain, redness, immobility (loss of function), swelling and heat. Inflammation_sentence_21

The traditional names for signs of inflammation come from Latin: Inflammation_sentence_22


  • Dolor (pain)Inflammation_item_0_0
  • Calor (heat)Inflammation_item_0_1
  • Rubor (redness)Inflammation_item_0_2
  • Tumor (swelling)Inflammation_item_0_3
  • Functio laesa (loss of function)Inflammation_item_0_4

The first four (classical signs) were described by Celsus (ca. 30 BC–38 AD), while loss of function was probably added later by Galen. Inflammation_sentence_23

However, the addition of this fifth sign has also been ascribed to Thomas Sydenham and Virchow. Inflammation_sentence_24

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. Inflammation_sentence_25

Loss of function has multiple causes. Inflammation_sentence_26

Acute inflammation of the lung (usually caused in response to pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings. Inflammation_sentence_27

Process of acute inflammation Inflammation_section_3

The process of acute inflammation is initiated by resident immune cells already present in the involved tissue, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells and mast cells. Inflammation_sentence_28

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). Inflammation_sentence_29

PAMPs are compounds that are associated with various pathogens, but which are distinguishable from host molecules. Inflammation_sentence_30

DAMPs are compounds that are associated with host-related injury and cell damage. Inflammation_sentence_31

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. Inflammation_sentence_32

Vasodilation and its resulting increased blood flow causes the redness (rubor) and increased heat (calor). Inflammation_sentence_33

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). Inflammation_sentence_34

Some of the released mediators such as bradykinin increase the sensitivity to pain (hyperalgesia, dolor). Inflammation_sentence_35

The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly neutrophils and macrophages, outside of the blood vessels (extravasation) into the tissue. Inflammation_sentence_36

The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury. Inflammation_sentence_37

The loss of function (functio laesa) is probably the result of a neurological reflex in response to pain. Inflammation_sentence_38

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. Inflammation_sentence_39

These include the complement system activated by bacteria and the coagulation and fibrinolysis systems activated by necrosis, e.g. a burn or a trauma. Inflammation_sentence_40

Acute inflammation may be regarded as the first line of defense against injury. Inflammation_sentence_41

Acute inflammatory response requires constant stimulation to be sustained. Inflammation_sentence_42

Inflammatory mediators are short-lived and are quickly degraded in the tissue. Inflammation_sentence_43

Hence, acute inflammation begins to cease once the stimulus has been removed. Inflammation_sentence_44

Vascular component Inflammation_section_4

Vasodilation and increased permeability Inflammation_section_5

As defined, acute inflammation is an immunovascular response to an inflammatory stimulus. Inflammation_sentence_45

This means acute inflammation can be broadly divided into a vascular phase that occurs first, followed by a cellular phase involving immune cells (more specifically myeloid granulocytes in the acute setting). Inflammation_sentence_46

The vascular component of acute inflammation involves the movement of plasma fluid, containing important proteins such as fibrin and immunoglobulins (antibodies), into inflamed tissue. Inflammation_sentence_47

Upon contact with PAMPs, tissue macrophages and mastocytes release vasoactive amines such as histamine and serotonin, as well as eicosanoids such as prostaglandin E2 and leukotriene B4 to remodel the local vasculature. Inflammation_sentence_48

Macrophages and endothelial cells release nitric oxide. Inflammation_sentence_49

These mediators vasodilate and permeabilize the blood vessels, which results in the net distribution of blood plasma from the vessel into the tissue space. Inflammation_sentence_50

The increased collection of fluid into the tissue causes it to swell (edema). Inflammation_sentence_51

This exuded tissue fluid contains various antimicrobial mediators from the plasma such as complement, lysozyme, antibodies, which can immediately deal damage to microbes, and opsonise the microbes in preparation for the cellular phase. Inflammation_sentence_52

If the inflammatory stimulus is a lacerating wound, exuded platelets, coagulants, plasmin and kinins can clot the wounded area and provide haemostasis in the first instance. Inflammation_sentence_53

These clotting mediators also provide a structural staging framework at the inflammatory tissue site in the form of a fibrin lattice – as would construction scaffolding at a construction site – for the purpose of aiding phagocytic debridement and wound repair later on. Inflammation_sentence_54

Some of the exuded tissue fluid is also funnelled by lymphatics to the regional lymph nodes, flushing bacteria along to start the recognition and attack phase of the adaptive immune system. Inflammation_sentence_55

Acute inflammation is characterized by marked vascular changes, including vasodilation, increased permeability and increased blood flow, which are induced by the actions of various inflammatory mediators. Inflammation_sentence_56

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. Inflammation_sentence_57

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. Inflammation_sentence_58

Stasis allows leukocytes to marginate (move) along the endothelium, a process critical to their recruitment into the tissues. Inflammation_sentence_59

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. Inflammation_sentence_60

Plasma cascade systems Inflammation_section_6


  • The complement system, when activated, creates a cascade of chemical reactions that promotes opsonization, chemotaxis, and agglutination, and produces the MAC.Inflammation_item_1_5
  • The kinin system generates proteins capable of sustaining vasodilation and other physical inflammatory effects.Inflammation_item_1_6
  • The coagulation system or clotting cascade, which forms a protective protein mesh over sites of injury.Inflammation_item_1_7
  • The fibrinolysis system, which acts in opposition to the coagulation system, to counterbalance clotting and generate several other inflammatory mediators.Inflammation_item_1_8

Plasma-derived mediators Inflammation_section_7

  • non-exhaustive list Inflammation_sentence_61


NameInflammation_header_cell_2_0_0 Produced byInflammation_header_cell_2_0_1 DescriptionInflammation_header_cell_2_0_2
BradykininInflammation_cell_2_1_0 Kinin systemInflammation_cell_2_1_1 A vasoactive protein that is able to induce vasodilation, increase vascular permeability, cause smooth muscle contraction, and induce pain.Inflammation_cell_2_1_2
C3Inflammation_cell_2_2_0 Complement systemInflammation_cell_2_2_1 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.Inflammation_cell_2_2_2
C5aInflammation_cell_2_3_0 Complement systemInflammation_cell_2_3_1 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.Inflammation_cell_2_3_2
Factor XII (Hageman Factor)Inflammation_cell_2_4_0 LiverInflammation_cell_2_4_1 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.Inflammation_cell_2_4_2
Membrane attack complexInflammation_cell_2_5_0 Complement systemInflammation_cell_2_5_1 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.Inflammation_cell_2_5_2
PlasminInflammation_cell_2_6_0 Fibrinolysis systemInflammation_cell_2_6_1 Able to break down fibrin clots, cleave complement protein C3, and activate Factor XII.Inflammation_cell_2_6_2
ThrombinInflammation_cell_2_7_0 Coagulation systemInflammation_cell_2_7_1 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.Inflammation_cell_2_7_2

Cellular component Inflammation_section_8

The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Inflammation_sentence_62

Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Inflammation_sentence_63

Others release enzymatic granules that damage pathogenic invaders. Inflammation_sentence_64

Leukocytes also release inflammatory mediators that develop and maintain the inflammatory response. Inflammation_sentence_65

In general, acute inflammation is mediated by granulocytes, whereas chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes. Inflammation_sentence_66

Leukocyte extravasation Inflammation_section_9

Main article: Leukocyte extravasation Inflammation_sentence_67

Various leukocytes, particularly neutrophils, are critically involved in the initiation and maintenance of inflammation. Inflammation_sentence_68

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. Inflammation_sentence_69

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: Inflammation_sentence_70


  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. Activated macrophages in the tissue release cytokines such as IL-1 and TNFα, which in turn leads to production of chemokines that bind to proteoglycans forming gradient in the inflamed tissue and along the endothelial wall. Inflammatory cytokines induce the immediate expression of P-selectin on endothelial cell surfaces and P-selectin binds weakly to carbohydrate ligands on the surface of leukocytes and causes them to "roll" along the endothelial surface as bonds are made and broken. Cytokines released from injured cells induce the expression of E-selectin on endothelial cells, which functions similarly to P-selectin. Cytokines also induce the expression of integrin ligands such as ICAM-1 and VCAM-1 on endothelial cells, which mediate the adhesion and further slow leukocytes down. These weakly bound leukocytes are free to detach if not activated by chemokines produced in injured tissue after signal transduction via respective 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.Inflammation_item_2_9
  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.Inflammation_item_2_10
  3. Movement of leukocytes within the tissue via chemotaxis: Leukocytes reaching the tissue interstitium bind to extracellular matrix proteins via expressed integrins and CD44 to prevent them from leaving the site. A variety of molecules behave as chemoattractants, for example, C3a or C5, and cause the leukocytes to move along a chemotactic gradient towards the source of inflammation.Inflammation_item_2_11

Phagocytosis Inflammation_section_10

Main article: Phagocyte Inflammation_sentence_71

Extravasated neutrophils in the cellular phase come into contact with microbes at the inflamed tissue. Inflammation_sentence_72

Phagocytes express cell-surface endocytic pattern recognition receptors (PRRs) that have affinity and efficacy against non-specific microbe-associated molecular patterns (PAMPs). Inflammation_sentence_73

Most PAMPs that bind to endocytic PRRs and initiate phagocytosis are cell wall components, including complex carbohydrates such as mannans and β-glucans, lipopolysaccharides (LPS), peptidoglycans, and surface proteins. Inflammation_sentence_74

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. Inflammation_sentence_75

Upon endocytic PRR binding, actin-myosin cytoskeletal rearrangement adjacent to the plasma membrane occurs in a way that endocytoses the plasma membrane containing the PRR-PAMP complex, and the microbe. Inflammation_sentence_76

Phosphatidylinositol and Vps34-Vps15-Beclin1 signalling pathways have been implicated to traffic the endocytosed phagosome to intracellular lysosomes, where fusion of the phagosome and the lysosome produces a phagolysosome. Inflammation_sentence_77

The reactive oxygen species, superoxides and hypochlorite bleach within the phagolysosomes then kill microbes inside the phagocyte. Inflammation_sentence_78

Phagocytic efficacy can be enhanced by opsonization. Inflammation_sentence_79

Plasma derived complement C3b and antibodies that exude into the inflamed tissue during the vascular phase bind to and coat the microbial antigens. Inflammation_sentence_80

As well as endocytic PRRs, phagocytes also express opsonin receptors Fc receptor and complement receptor 1 (CR1), which bind to antibodies and C3b, respectively. Inflammation_sentence_81

The co-stimulation of endocytic PRR and opsonin receptor increases the efficacy of the phagocytic process, enhancing the lysosomal elimination of the infective agent. Inflammation_sentence_82

Cell-derived mediators Inflammation_section_11

  • non-exhaustive list Inflammation_sentence_83


NameInflammation_header_cell_3_0_0 TypeInflammation_header_cell_3_0_1 SourceInflammation_header_cell_3_0_2 DescriptionInflammation_header_cell_3_0_3
Lysosome granulesInflammation_cell_3_1_0 EnzymesInflammation_cell_3_1_1 GranulocytesInflammation_cell_3_1_2 These cells contain a large variety of enzymes that 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 that allow these enzymes to act as inflammatory mediators.Inflammation_cell_3_1_3
HistamineInflammation_cell_3_2_0 MonoamineInflammation_cell_3_2_1 Mast cells and basophilsInflammation_cell_3_2_2 Stored in preformed granules, histamine is released in response to a number of stimuli. It causes arteriole dilation, increased venous permeability, and a wide variety of organ-specific effects.Inflammation_cell_3_2_3
IFN-γInflammation_cell_3_3_0 CytokineInflammation_cell_3_3_1 T-cells, NK cellsInflammation_cell_3_3_2 Antiviral, immunoregulatory, and anti-tumour properties. This interferon was originally called macrophage-activating factor, and is especially important in the maintenance of chronic inflammation.Inflammation_cell_3_3_3
IL-8Inflammation_cell_3_4_0 ChemokineInflammation_cell_3_4_1 Primarily macrophagesInflammation_cell_3_4_2 Activation and chemoattraction of neutrophils, with a weak effect on monocytes and eosinophils.Inflammation_cell_3_4_3
Leukotriene B4Inflammation_cell_3_5_0 EicosanoidInflammation_cell_3_5_1 Leukocytes, cancer cellsInflammation_cell_3_5_2 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.Inflammation_cell_3_5_3
LTC4, LTD4Inflammation_cell_3_6_0 EicosanoidInflammation_cell_3_6_1 eosinophils, mast cells, macrophagesInflammation_cell_3_6_2 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.Inflammation_cell_3_6_3
5-oxo-eicosatetraenoic acidInflammation_cell_3_7_0 EicosanoidInflammation_cell_3_7_1 leukocytes, cancer cellsInflammation_cell_3_7_2 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.Inflammation_cell_3_7_3
5-HETEInflammation_cell_3_8_0 EicosanoidInflammation_cell_3_8_1 LeukocytesInflammation_cell_3_8_2 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.Inflammation_cell_3_8_3
ProstaglandinsInflammation_cell_3_9_0 EicosanoidInflammation_cell_3_9_1 Mast cellsInflammation_cell_3_9_2 A group of lipids that can cause vasodilation, fever, and pain.Inflammation_cell_3_9_3
Nitric oxideInflammation_cell_3_10_0 Soluble gasInflammation_cell_3_10_1 Macrophages, endothelial cells, some neuronsInflammation_cell_3_10_2 Potent vasodilator, relaxes smooth muscle, reduces platelet aggregation, aids in leukocyte recruitment, direct antimicrobial activity in high concentrations.Inflammation_cell_3_10_3
TNF-α and IL-1Inflammation_cell_3_11_0 CytokinesInflammation_cell_3_11_1 Primarily macrophagesInflammation_cell_3_11_2 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.Inflammation_cell_3_11_3
TryptaseInflammation_cell_3_12_0 EnzymesInflammation_cell_3_12_1 Mast CellsInflammation_cell_3_12_2 This serine protease is believed to be exclusively stored in mast cells and secreted, along with histamine, during mast cell activation.Inflammation_cell_3_12_3

Morphologic patterns Inflammation_section_12

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. Inflammation_sentence_84


  • Granulomatous inflammation: Characterised by the formation of granulomas, they are the result of a limited but diverse number of diseases, which include among others tuberculosis, leprosy, sarcoidosis, and syphilis.Inflammation_item_3_12
  • Fibrinous inflammation: Inflammation resulting in a large increase in vascular permeability allows fibrin to pass through the blood vessels. If an appropriate procoagulative stimulus is present, such as cancer cells, a fibrinous exudate is deposited. This is commonly seen in serous cavities, where the conversion of fibrinous exudate into a scar can occur between serous membranes, limiting their function. The deposit sometimes forms a pseudomembrane sheet. During inflammation of the intestine (Pseudomembranous colitis), pseudomembranous tubes can be formed.Inflammation_item_3_13
  • Purulent inflammation: Inflammation resulting in large amount of pus, which consists of neutrophils, dead cells, and fluid. Infection by pyogenic bacteria such as staphylococci is characteristic of this kind of inflammation. Large, localised collections of pus enclosed by surrounding tissues are called abscesses.Inflammation_item_3_14
  • Serous inflammation: Characterised by the copious effusion of non-viscous serous fluid, commonly produced by mesothelial cells of serous membranes, but may be derived from blood plasma. Skin blisters exemplify this pattern of inflammation.Inflammation_item_3_15
  • Ulcerative inflammation: Inflammation occurring near an epithelium can result in the necrotic loss of tissue from the surface, exposing lower layers. The subsequent excavation in the epithelium is known as an ulcer.Inflammation_item_3_16

Inflammatory disorders Inflammation_section_13

Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. Inflammation_sentence_85

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. Inflammation_sentence_86

Non-immune diseases with causal origins in inflammatory processes include cancer, atherosclerosis, and ischemic heart disease. Inflammation_sentence_87

Examples of disorders associated with inflammation include: Inflammation_sentence_88

Atherosclerosis Inflammation_section_14

Main article: Atherosclerosis Inflammation_sentence_89

Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Inflammation_sentence_90

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. Inflammation_sentence_91

These new findings provide important links between risk factors and the mechanisms of atherogenesis. Inflammation_sentence_92

Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Inflammation_sentence_93

Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. Inflammation_sentence_94

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. Inflammation_sentence_95

Moreover, certain treatments that reduce coronary risk also limit inflammation. Inflammation_sentence_96

In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. Inflammation_sentence_97

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. Inflammation_sentence_98

Allergy Inflammation_section_15

An allergic reaction, formally known as type 1 hypersensitivity, is the result of an inappropriate immune response triggering inflammation, vasodilation, and nerve irritation. Inflammation_sentence_99

A common example is hay fever, which is caused by a hypersensitive response by mast cells to allergens. Inflammation_sentence_100

Pre-sensitised mast cells respond by degranulating, releasing vasoactive chemicals such as histamine. Inflammation_sentence_101

These chemicals propagate an excessive inflammatory response characterised by blood vessel dilation, production of pro-inflammatory molecules, cytokine release, and recruitment of leukocytes. Inflammation_sentence_102

Severe inflammatory response may mature into a systemic response known as anaphylaxis. Inflammation_sentence_103

Myopathies Inflammation_section_16

Inflammatory myopathies are caused by the immune system inappropriately attacking components of muscle, leading to signs of muscle inflammation. Inflammation_sentence_104

They may occur in conjunction with other immune disorders, such as systemic sclerosis, and include dermatomyositis, polymyositis, and inclusion body myositis. Inflammation_sentence_105

Leukocyte defects Inflammation_section_17

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. Inflammation_sentence_106

Dysfunctional leukocytes may be unable to correctly bind to blood vessels due to surface receptor mutations, digest bacteria (Chédiak–Higashi syndrome), or produce microbicides (chronic granulomatous disease). Inflammation_sentence_107

In addition, diseases affecting the bone marrow may result in abnormal or few leukocytes. Inflammation_sentence_108

Pharmacological Inflammation_section_18

Certain drugs or exogenous chemical compounds are known to affect inflammation. Inflammation_sentence_109

Vitamin A deficiency causes an increase in inflammatory responses, and anti-inflammatory drugs work specifically by inhibiting the enzymes that produce inflammatory eicosanoids. Inflammation_sentence_110

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). Inflammation_sentence_111

Cancer Inflammation_section_19

Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration. Inflammation_sentence_112

Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis. Inflammation_sentence_113

On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer. Inflammation_sentence_114

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. Inflammation_sentence_115

This capacity of a mediator of inflammation to influence the effects of steroid hormones in cells, is very likely to affect carcinogenesis on the one hand; 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. Inflammation_sentence_116

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. Inflammation_sentence_117

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. Inflammation_sentence_118

Role in cancer Inflammation_section_20

In 1863, Rudolf Virchow hypothesized that the origin of cancer was at sites of chronic inflammation. Inflammation_sentence_119

At present, chronic inflammation is estimated to contribute to approximately 15% to 25% of human cancers. Inflammation_sentence_120

Mediators and DNA damage in cancer Inflammation_section_21

An inflammatory mediator is a messenger that acts on blood vessels and/or cells to promote an inflammatory response. Inflammation_sentence_121

Inflammatory mediators that contribute to neoplasia include prostaglandins, inflammatory cytokines such as IL-1β, TNF-α, IL-6 and IL-15 and chemokines such as IL-8 and GRO-alpha. Inflammation_sentence_122

These inflammatory mediators, and others, orchestrate an environment that fosters proliferation and survival. Inflammation_sentence_123

Inflammation also causes DNA damages due to the induction of reactive oxygen species (ROS) by various intracellular inflammatory mediators. Inflammation_sentence_124

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). Inflammation_sentence_125

ROS and RNS are normally produced by these cells to fight infection. Inflammation_sentence_126

ROS, alone, cause more than 20 types of DNA damage. Inflammation_sentence_127

Oxidative DNA damages cause both mutations and epigenetic alterations. Inflammation_sentence_128

RNS also cause mutagenic DNA damages. Inflammation_sentence_129

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. Inflammation_sentence_130

DNA damages may cause genetic mutations due to inaccurate repair. Inflammation_sentence_131

In addition, mistakes in the DNA repair process may cause epigenetic alterations. Inflammation_sentence_132

Mutations and epigenetic alterations that are replicated and provide a selective advantage during somatic cell proliferation may be carcinogenic. Inflammation_sentence_133

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. Inflammation_sentence_134

However, chronic inflammation also causes epigenetic changes such as DNA methylations, that are often more common than mutations. Inflammation_sentence_135

Typically, several hundreds to thousands of genes are methylated in a cancer cell (see DNA methylation in cancer). Inflammation_sentence_136

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. Inflammation_sentence_137

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). Inflammation_sentence_138

DNA repair genes, in particular, are frequently inactivated by methylation in various cancers (see hypermethylation of DNA repair genes in cancer). Inflammation_sentence_139

A 2018 report evaluated the relative importance of mutations and epigenetic alterations in progression to two different types of cancer. Inflammation_sentence_140

This report showed that epigenetic alterations were much more important than mutations in generating gastric cancers (associated with inflammation). Inflammation_sentence_141

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). Inflammation_sentence_142

HIV and AIDS Inflammation_section_22

It has long been recognized that infection with HIV is characterized not only by development of profound immunodeficiency but also by sustained inflammation and immune activation. Inflammation_sentence_143

A substantial body of evidence implicates chronic inflammation as a critical driver of immune dysfunction, premature appearance of aging-related diseases, and immune deficiency. Inflammation_sentence_144

Many now regard HIV infection not only as an evolving virus-induced immunodeficiency but also as chronic inflammatory disease. Inflammation_sentence_145

Even after the introduction of effective antiretroviral therapy (ART) and effective suppression of viremia in HIV-infected individuals, chronic inflammation persists. Inflammation_sentence_146

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. Inflammation_sentence_147

This lack of pathogenicity is accompanied by a lack of inflammation, immune activation and cellular proliferation. Inflammation_sentence_148

In sharp contrast, experimental SIVsm infection of rhesus macaque produces immune activation and AIDS-like disease with many parallels to human HIV infection. Inflammation_sentence_149

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. Inflammation_sentence_150

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. Inflammation_sentence_151

These are the two signature events that propel HIV disease progression to AIDS. Inflammation_sentence_152

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. Inflammation_sentence_153

The feed-forward nature of this inflammatory response produces chronic inflammation and tissue injury. Inflammation_sentence_154

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. Inflammation_sentence_155

In this regard, pyroptosis of CD4 T cells and secretion of pro-inflmammatory 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, which has already proven to be safe and well tolerated in phase II human clinical trials. Inflammation_sentence_156

These findings could propel development of an entirely new class of “anti-AIDS” therapies that act by targeting the host rather than the virus. Inflammation_sentence_157

Such agents would almost certainly be used in combination with ART. Inflammation_sentence_158

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. Inflammation_sentence_159

Resolution of inflammation Inflammation_section_23

The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues. Inflammation_sentence_160

Failure to do so results in chronic inflammation, and cellular destruction. Inflammation_sentence_161

Resolution of inflammation occurs by different mechanisms in different tissues. Inflammation_sentence_162

Mechanisms that serve to terminate inflammation include: Inflammation_sentence_163

Connection to depression Inflammation_section_24

There is evidence for a link between inflammation and depression. Inflammation_sentence_164

Inflammatory processes can be triggered by negative cognitions or their consequences, such as stress, violence, or deprivation. Inflammation_sentence_165

Thus, negative cognitions can cause inflammation that can, in turn, lead to depression. Inflammation_sentence_166

In addition there is increasing evidence that inflammation can cause depression because of the increase of cytokines, setting the brain into a "sickness mode". Inflammation_sentence_167

Classical symptoms of being physically sick like lethargy show a large overlap in behaviors that characterize depression. Inflammation_sentence_168

Levels of cytokines tend to increase sharply during the depressive episodes of people with bipolar disorder and drop off during remission. Inflammation_sentence_169

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. Inflammation_sentence_170

Inflammations that lead to serious depression could be caused by common infections such as those caused by a virus, bacteria or even parasites. Inflammation_sentence_171

Systemic effects Inflammation_section_25

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. Inflammation_sentence_172

If an organism is not contained by the actions of acute inflammation it may gain access to the lymphatic system via nearby lymph vessels. Inflammation_sentence_173

An infection of the lymph vessels is known as lymphangitis, and infection of a lymph node is known as lymphadenitis. Inflammation_sentence_174

When lymph nodes cannot destroy all pathogens, the infection spreads further. Inflammation_sentence_175

A pathogen can gain access to the bloodstream through lymphatic drainage into the circulatory system. Inflammation_sentence_176

When inflammation overwhelms the host, systemic inflammatory response syndrome is diagnosed. Inflammation_sentence_177

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. Inflammation_sentence_178

Vasodilation and organ dysfunction are serious problems associated with widespread infection that may lead to septic shock and death. Inflammation_sentence_179

Acute-phase proteins Inflammation_section_26

Inflammation also induces high systemic levels of acute-phase proteins. Inflammation_sentence_180

In acute inflammation, these proteins prove beneficial; however, in chronic inflammation they can contribute to amyloidosis. Inflammation_sentence_181

These proteins include C-reactive protein, serum amyloid A, and serum amyloid P, which cause a range of systemic effects including: Inflammation_sentence_182

Leukocyte numbers Inflammation_section_27

Inflammation often affects the numbers of leukocytes present in the body: Inflammation_sentence_183


  • Leukocytosis is often seen during inflammation induced by infection, where it results in a large increase in the amount of leukocytes in the blood, especially immature cells. Leukocyte numbers usually increase to between 15 000 and 20 000 cells per microliter, but extreme cases can see it approach 100 000 cells per microliter. Bacterial infection usually results in an increase of neutrophils, creating neutrophilia, whereas diseases such as asthma, hay fever, and parasite infestation result in an increase in eosinophils, creating eosinophilia.Inflammation_item_4_17
  • Leukopenia can be induced by certain infections and diseases, including viral infection, Rickettsia infection, some protozoa, tuberculosis, and some cancers.Inflammation_item_4_18

Systemic inflammation and obesity Inflammation_section_28

With the discovery of interleukins (IL), the concept of systemic inflammation developed. Inflammation_sentence_184

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. Inflammation_sentence_185

Chronic inflammation is widely observed in obesity. Inflammation_sentence_186

Obese people commonly have many elevated markers of inflammation, including: Inflammation_sentence_187


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. Inflammation_sentence_188

Waist circumference correlates significantly with systemic inflammatory response. Inflammation_sentence_189

Loss of white adipose tissue reduces levels of inflammation markers. Inflammation_sentence_190

The association of systemic inflammation with insulin resistance and type 2 diabetes, and with atherosclerosis is under preliminary research, although rigorous clinical trials have not been conducted to confirm such relationships. Inflammation_sentence_191

C-reactive protein (CRP) is generated at a higher level in obese people, and may increase the risk for cardiovascular diseases. Inflammation_sentence_192

Outcomes Inflammation_section_29

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. Inflammation_sentence_193

Here are the possible outcomes to inflammation: Inflammation_sentence_194


  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. In situations where limited or short-lived inflammation has occurred this is usually the outcome.Inflammation_item_6_20
  2. Fibrosis Large amounts of tissue destruction, or damage in tissues unable to regenerate, cannot be regenerated completely by the body. Fibrous 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.Inflammation_item_6_21
  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.Inflammation_item_6_22
  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_item_6_23

Examples Inflammation_section_30

Inflammation is usually indicated by adding the suffix "", as shown below. Inflammation_sentence_195

However, some conditions such as asthma and pneumonia do not follow this convention. Inflammation_sentence_196

More examples are available at list of types of inflammation. Inflammation_sentence_197


  • Inflammation_item_7_24
  • Inflammation_item_7_25
  • Inflammation_item_7_26
  • Inflammation_item_7_27

See also Inflammation_section_31

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