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How the Inflammation Event Occurs

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Inflammation is the response of the body's vascularized tissues to harmful stimuli such as infectious agents, mechanical damage, chemical irritants, etc. Inflammation has both local and systemic manifestations and may be either acute or chronic

Local inflammatory response (local inflammation) occurs within the area affected by the harmful stimulus. Acute local inflammation develops within minutes or hours after the influence of a harmful stimulus, has a short duration, and primarily involves the innate immune system. The five classic signs of acute local inflammation are redness, swelling, heat, pain, and loss of function. These classical signs result from the sequence of events that are triggered by tissue damage and allow leukocytes to get to the site of damage to eliminate the causative factor.

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These key events mentioned above will be enhanced by actions of mediators. Mediators in inflammation include prostaglandins, leukotrienes, vasoactive amines (such as histamine), plasma kinins (such as bradykinin), cytokines (such as tumour necrosis factors and interleukins) and complement – derived peptide mediators. The most relevant of the polypeptide mediators jointly known as cytokines are tumour necrosis factor (TNF) which is synthesised primarily by macrophages and interleukin 1 (IL-1) which is made by various cells but likely to be produced by macrophage lineage, epithelial and endothelial cells at the early stages of inflammation. The functions of these two cytokines overlap although relative potencies with cell type and biological effect may differ. The functions of these cytokines can be observed in three main areas namely (i) defence role, (ii) repair role and (iii) metabolic role. Histamine as a mediator of inflammation plays a major role in acute inflammatory response affiliated with mast cell degranulation. It is primarily stored and released from mast cells normally found along blood vessels. The release of histamine leads to the following responses; (i) increased microvascular permeability leading to oedema formation, (ii) increase in blood flow and volume and (iii) vasodilatation in the skin as a result of local axon reflex. The combined effect of the increased microvascular permeability and part of the hydrostatic segment of the vasodilatation response caused by histamine mainly contributes to oedema formation. The two main receptors involved in the acute inflammatory response are H1 and H2 receptors, both receptors are involved in vasodilatation while increased microvascular permeability only utilises the H1 receptor. Histamine lacks chemotactic activity however; they may be specifically chemotactic towards eosinophils. The permeability of microcirculation is also increased by histamine allowing the movement of white blood cells into the extravascular space, the amount of white blood cells moved into the extravascular space is however insignificant compared to other inflammatory processes. Our understanding of atherosclerosis is that it’s this disease that involves simply passive accumulation of lipids in the artery; furthermore in addition, it is also an inflammatory disease involving a number of factors and stages. Each stage of this disease from initiation to termination involves inflammation; inflammatory response is enhanced in this disease as the homeostatic functions are altered. The inflammation of the endothelial walls in the artery attracts leucocytes and monocytes which penetrates the intima resulting into predisposition of the artery wall to lipid vasculitis. Another event that happens is the migration of the T cells into the intima where it secretes cytokines which are responsible for promoting inflammatory response, which also further enhances the proliferation of smooth muscle cells. Inflammatory mediator can also weaken the protective cap of the atheroma resulting into thrombosis and a possible appearance of acute coronary syndrome such as myocardial infarction and angina pectoris.

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Inflammation is the immune system's response to harmful stimuli, such as pathogens, damaged cells, toxic compounds, or irradiation, and acts by removing injurious stimuli and initiating the healing process. Inflammation is therefore a defense mechanism that is vital to health

Usually, during acute inflammatory responses, cellular and molecular events and interactions efficiently minimize impending injury or infection. This mitigation process contributes to restoration of tissue homeostasis and resolution of the acute inflammation. However, uncontrolled acute inflammation may become chronic, contributing to a variety of chronic inflammatory diseases. At the tissue level, inflammation is characterized by redness, swelling, heat, pain, and loss of tissue function, which result from local immune, vascular and inflammatory cell responses to infection or injury. Important microcirculatory events that occur during the inflammatory process include vascular permeability changes, leukocyte recruitment and accumulation, and inflammatory mediator release. Various pathogenic factors, such as infection, tissue injury, or cardiac infarction, can induce inflammation by causing tissue damage. The etiologies of inflammation can be infectious or non-infectious. In response to tissue injury, the body initiates a chemical signaling cascade that stimulates responses aimed at healing affected tissues (Medzhitov R., 2010). These signals activate leukocyte chemotaxis from the general circulation to sites of damage. These activated leukocytes produce cytokines that induce inflammatory responses. The inflammatory response is the coordinate activation of signaling pathways that regulate inflammatory mediator levels in resident tissue cells and inflammatory cells recruited from the blood [8]. Inflammation is a common pathogenesis of many chronic diseases, including cardiovascular and bowel diseases, diabetes, arthritis, and cancer [9]. Although inflammatory response processes depend on the precise nature of the initial stimulus and its location in the body, they all share a common mechanism, which can be summarized as follows: 1) cell surface pattern receptors recognize detrimental stimuli; 2) inflammatory pathways are activated; 3) inflammatory markers are released; and 4) inflammatory cells are recruited (Zhou Y, Hong Y, 2016).

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As can be seen, when a wound swells up, turns red and hurts, it may be a sign of inflammation. Very generally speaking, inflammation is the body’s immune system’s response to an irritant

The irritant might be a germ, but it could also be a foreign object, such as a splinter in your finger. This means that an inflammation doesn’t only start when, for instance, a wound has already been infected by bacteria, is oozing pus or healing poorly. It already starts when the body is trying to fight against the harmful irritant.

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Medzhitov R. Inflammation 2010: new adventures of an old flame. Cell. 2010;140:771–776.

Ferrero-Miliani L, Nielsen O, Andersen P, Girardin S. Chronic inflammation: importance of NOD2 and NALP3 in interleukin-1β generation. Clin Exp Immunol. 2007;147:227–235.

Nathan C, Ding A. Nonresolving inflammation. Cell. 2010;140:871–882.

Zhou Y, Hong Y, Huang H. Triptolide Attenuates Inflammatory Response in Membranous Glomerulo-Nephritis Rat via Downregulation of NF-κB Signaling Pathway. Kidney and Blood Pressure Res. 2016;41:901–910.

Takeuchi O, Akira S. Pattern Recognition Receptors and Inflammation. Cell. 2010

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