Inflammation (from inflammatio]]) is part of the biological response of body tissues to harmful stimuli, such as , damaged cells, or Irritation.
Inflammation is a generic response, and therefore is considered a mechanism of innate immunity, whereas adaptive immunity is specific to each pathogen.
Inflammation is a protective response involving immune cells, , and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out damaged cells and tissues, and initiate tissue repair. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. However inflammation can also have negative effects.
Inflammation can be classified as acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli, and is achieved by the increased movement of blood plasma and (in particular ) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells in 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, such as mononuclear cells, and involves simultaneous destruction and healing of the tissue.
Inflammation has also been classified as Type 1 and Type 2 based on the type of cytokines and helper T cells (Th1 and Th2) involved.
Meaning
The earliest known reference for the term inflammation is around the early 15th century. The word root comes from
Old French inflammation around the 14th century, which then comes from
Latin inflammatio or
inflammationem. Literally, the term relates to the word "flame", as the property of being "set on fire" or "to burn".
The term 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 in discussion of infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation, on the other hand, describes just the body's immunovascular response, regardless of cause. But, because of the two are often correlation, words ending in the suffix (which means 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 is crucial in situations in pathology and medical diagnosis that involve inflammation that is not driven by microbial invasion, such as cases of atherosclerosis, trauma, ischemia, and autoimmune diseases (including type III hypersensitivity).
Causes
Types
| + Comparison between acute and chronic inflammation:
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Acute
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.
It involves a coordinated and systemic mobilization response locally of various immune, endocrine and neurological mediators of acute inflammation. In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and then ceases.
Acute inflammation occurs immediately upon injury, lasting only a few days.
Cardinal signs
Inflammation is characterized by five cardinal signs,
The first four (classical signs) were described by Celsus (–38 AD).
Pain is due to the release of chemicals such as bradykinin and histamine that stimulate nerve endings.
Loss of function
The fifth sign,
loss of function, is believed to have been added later by
Galen,
or Rudolf Virchow.
Examples of loss of function include pain that inhibits mobility, severe swelling that prevents movement, having a worse sense of smell during a cold, or having difficulty breathing when bronchitis is present.
Loss of function has multiple causes.
Acute process
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
. 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
, 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 blood 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 and macrophages, to flow out of the blood vessels (extravasation) and into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury.
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., burn, trauma).
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.
Chronic
Chronic inflammation is inflammation that lasts for months or years.
Macrophages,
lymphocytes, and
plasma cells predominate in chronic inflammation, in contrast to the neutrophils that predominate in acute inflammation.
Diabetes, cardiovascular disease,
Allergy, and chronic obstructive pulmonary disease (COPD) are examples of diseases mediated by chronic inflammation.
, smoking, stress and insufficient diet are some of the factors that promote chronic inflammation.
A 2014 study reported that 60% of Americans had at least one chronic inflammatory condition, and 42% had more than one.
Cardinal signs
Common signs and symptoms that develop during chronic inflammation are:
-
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.
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).
The vascular component of acute inflammation involves the movement of
Blood plasma, containing important
such as
fibrin and
(
antibodies), into inflamed tissue.
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.
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.
Plasma cascade systems
-
The complement system, when activated, creates a cascade of chemical reactions that promotes opsonization, chemotaxis, and agglutination, and produces the MAC.
-
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
|
| A vasoactive protein that is able to induce vasodilation, increase vascular permeability, cause smooth muscle contraction, and induce pain. |
| 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. |
| 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. |
| 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. |
| 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. |
| Able to break down fibrin clots, cleave complement protein C3, and activate Factor XII. |
| 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 and nitric oxide. |
Cellular component
The
cellular component involves
, which normally reside in blood and must move into the inflamed tissue via
extravasation to aid in inflammation.
Some act as
, 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
, whereas chronic inflammation is mediated by mononuclear cells such as
and
.
Leukocyte extravasation
Various
, 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:
-
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.
-
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.
-
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 , for example, C3a or C5a (the anaphylatoxins), and cause the leukocytes to move along a chemotactic gradient towards the source of inflammation.
Phagocytosis
Extravasated neutrophils in the cellular phase come into contact with microbes at the inflamed tissue.
express cell-surface endocytic pattern recognition receptors (PRRs) that have affinity and efficacy against non-specific microbe-associated molecular patterns (PAMPs). 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. 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, actin-myosin cytoskeletal rearrangement adjacent to the plasma membrane occurs in a way that endocytosis the plasma membrane containing the PRR-PAMP complex, and the microbe. 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. The reactive oxygen species, superoxides and hypochlorite bleach within the phagolysosomes then kill microbes inside the phagocyte.
Phagocytic efficacy can be enhanced by opsonization. Plasma derived complement C3b and antibodies that exude into the inflamed tissue during the vascular phase bind to and coat the microbial antigens. As well as endocytic PRRs, phagocytes also express opsonin receptors Fc receptor and complement receptor 1 (CR1), which bind to antibodies and C3b, respectively. The co-stimulation of endocytic PRR and opsonin receptor increases the efficacy of the phagocytic process, enhancing the lysosomal elimination of the infective agent.
Cell-derived mediators
|
| These cells contain a large variety of enzymes that perform a number of functions. Granules can be classified as either specific or 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. |
| Elevated GM-CSF has been shown to contribute to inflammation in inflammatory arthritis, osteoarthritis, colitis asthma, obesity, and COVID-19. |
| 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. |
| Antiviral, immunoregulatory, and anti-tumour properties. This interferon was originally called macrophage-activating factor, and is especially important in the maintenance of chronic inflammation. |
| 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. |
| Activation and chemoattraction of neutrophils, with a weak effect on monocytes and eosinophils. |
| 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. |
| 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. |
| A group of lipids that can cause vasodilation, fever, and pain. |
| Potent vasodilator, relaxes smooth muscle, reduces platelet aggregation, aids in leukocyte recruitment, direct antimicrobial activity in high concentrations. |
| 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 . Responsible for the systemic effects of inflammation, such as loss of appetite and increased heart rate. TNF-α inhibits osteoblast differentiation. |
This serine protease is believed to be exclusively stored in mast cells and secreted, along with histamine, during mast cell activation. |
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
epithelial surface, or
pyogenic bacteria are involved.
-
Granulomatous inflammation: Characterised by the formation of , they are the result of a limited but diverse number of diseases, which include among others tuberculosis, leprosy, sarcoidosis, and syphilis.
-
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,
-
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 .
-
Serous inflammation: Characterised by the copious effusion of non-viscous serous fluid, commonly produced by mesothelial cells of , but may be derived from blood plasma. Skin exemplify this pattern of inflammation.
-
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.
Disorders
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 allergic reactions and some
myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with causal origins in inflammatory processes include cancer,
atherosclerosis, and ischemic heart disease.
Examples of disorders associated with inflammation include:
Atherosclerosis
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.
Allergy
An allergic reaction, formally known as type 1 hypersensitivity, is the result of an inappropriate immune response triggering inflammation, vasodilation, and nerve irritation. A common example is
hay fever, which is caused by a hypersensitive response by
to
. Pre-sensitised mast cells respond by
degranulation, 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.
Severe inflammatory response may mature into a systemic response known as
anaphylaxis.
Myopathies
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.
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.
Dysfunctional leukocytes may be unable to correctly bind to blood vessels due to surface receptor mutations, digest bacteria (Chédiak–Higashi syndrome), or produce
(chronic granulomatous disease). In addition, diseases affecting the
bone marrow may result in abnormal or few leukocytes.
Pharmacological
Certain drugs or exogenous chemical compounds are known to affect inflammation.
Vitamin A deficiency, for example, causes an increase in inflammatory responses,
and anti-inflammatory drugs work specifically by inhibiting the enzymes that produce inflammatory
eicosanoids. Additionally, 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).
Cancer
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.
On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.
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.
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.
Role in cancer
In 1863,
Rudolf Virchow hypothesized that the origin of cancer was at sites of chronic inflammation.
As of 2012, chronic inflammation was estimated to contribute to approximately 15% to 25% of human cancers.
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.
Inflammatory mediators that contribute to neoplasia include
, inflammatory
such as IL-1β, TNF-α, IL-6 and IL-15 and
such as IL-8 and GRO-alpha.
These inflammatory mediators, and others, orchestrate an environment that fosters proliferation and survival.
Inflammation also causes DNA damages due to the induction of reactive oxygen species (ROS) by various intracellular inflammatory mediators.
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 due to inaccurate repair. In addition, mistakes in the DNA repair process may cause epigenetic alterations.
Genome-wide analyses of human cancer tissues reveal that a single typical cancer cell may possess roughly 100 mutations in , 10–20 of which are carcinogenesis that contribute to cancer development.
HIV and AIDS
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.
A substantial body of evidence implicates chronic inflammation as a critical driver of immune dysfunction, premature appearance of aging-related diseases, and immune deficiency.
Many now regard HIV infection not only as an evolving virus-induced immunodeficiency, but also as chronic inflammatory disease.
Even after the introduction of 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: SIV
sm infection of its natural nonhuman primate hosts, the
sooty mangabey, causes high-level viral replication but limited evidence of disease.
This lack of pathogenicity is accompanied by a lack of inflammation, immune activation and cellular proliferation. In sharp contrast, experimental SIV
sm infection of
rhesus macaque produces immune activation and AIDS-like disease with many parallels to human HIV infection.
Delineating how CD4 T cells are depleted and how chronic inflammation and immune activation are induced lies at the heart of understanding HIV pathogenesisone 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.
Resolution
The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues.
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:
Connection to depression
There is evidence for a link between inflammation and depression.
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.
In addition, there is increasing evidence that inflammation can cause depression because of the increase of cytokines, setting the brain into a "sickness mode".
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.
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.
Systemic effects
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
. An infection of the lymph vessels is known as
lymphangitis, and infection of a lymph node is known as
lymphadenitis. 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, 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.
Acute-phase proteins
Inflammation also is characterized by high systemic levels of acute-phase proteins. In acute inflammation, these proteins prove beneficial; however, in chronic inflammation, they can contribute to
amyloidosis.
These proteins include C-reactive protein, serum amyloid A, and serum amyloid P, which cause a range of systemic effects including:
Leukocyte numbers
Inflammation often affects the numbers of leukocytes present in the body:
-
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.
-
Leukopenia can be induced by certain infections and diseases, including viral infection, Rickettsia infection, some protozoa, tuberculosis, and some cancers.
Interleukins and obesity
With the discovery of
(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.
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.
Loss of white adipose tissue reduces levels of inflammation markers.
C-reactive protein (CRP) is generated at a higher level in obese people, and may increase the risk for cardiovascular diseases.
Outcomes
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:
-
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 cells regenerate. Such is usually the outcome when limited or short-lived inflammation has occurred.
-
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 cells, hence functional impairment may occur.
-
Abscess formation
A cavity is formed containing pus, an opaque liquid containing dead white blood cells and bacteria with general debris from destroyed cells.
-
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 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.
Examples
Inflammation is usually indicated by adding the suffix "", 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.
See also
Notes
External links
