Initiation of Inflammation

Initiation of inflammation Inflammation is the result ofpoisoning, various conditions including infection, as physical trauma or injury, burns, allergies and hypersensitivity, well as autoimmune diseases which result in the release of pro-inflammatory mediators. The natural nature of pro-inflammatory mediators isandto cause aof series of reactions called the inflammatory response. The type degree damage asInflammation well as individual geneticbyfactors influence the inflammatory reaction. is initiated complex interactions involving chemical mediators.Some of them are derived from invading organisms, some are released by damaged tissue,thatfrom enzymes, from white blood cells. Some chemical mediators areplasma important to knowandinclude: 1.andHistamine cells after tissue damage and stimulates vasodilation increased(released capillarybypermeability) 2.contraction Lecotrin (produced fromchemotaxis cell membranes and increases smooth muscle and promotes for neutrophils) 3.vascular Prostaglandins (produced from cellchemotaxis membranes increase vasodilation, permeability and promote forand neutrophils) 4.chemotaxis Platelet aggregating factors (cause platelet aggregation and promote for neutrophils 5.traffic Chemokines (produced by various cellsseveral and acttypes as regulators of leukocyte at inflammatory sites). There are of chemokines, for T example: IL-8 (interleukin-8), RANTES (regulated upon activation of normal cell expressed and secreted), MCP (monocyte chemoattractant protein) 6.endogenous Cytokines pyrogens (producedthat by phagocytic cells at thethe sitehypothalamus, of inflammationtrigger and act as trigger fever through the production ofmarrow acute phase proteins by the liver,There triggerareincreased hematopoiesis by the bone resulting in leukocytosis). several types of cytokines, namely: IL-1 (interleukin-1), IL-6 (interleukin-6), TNF-a (tumor necrosis factor alpha).Other mediators (produced as nitric a resultoxide, of theperoxide phagocytosis process). There are several other mediators, namely and oxygen radicals. Oxygen and nitrogen are intermediates that are very toxic to microorganisms. Reaction to the Inflammatory Response The release of inflammatory mediatorscontents such asdue leukotrienes and is the prostaglandins as well as other cytoplasmic to cell damage initiation of thebyinflammatory reactioninflammation in trauma. Bacterial components and toxins released bacteria stimulate in infections. Degranulation ofrelease mast ofcells and activation ofmacrophages complementdigest due toparticles physicaland trauma causes the histamine. Tissue debris, making them active and Macrophages releasing a number of pro-inflammatory cytokines such as IL-1, IL-6 and TNF-a. also produce chemokines, where these chemokines can attract the attention histamine of special leukocytes to movecomponents to the site of infection or trauma. Prostaglandins, and complement (especially anaphylatoxins C3a and C5a) cause vasodilation and increase vascular permeability. Conditions of vascularwhere hyperpermeability increase fluid extravasation, including macromolecules, extravasation of macromolecules like this in normal vascular conditions is not possible.Monokines also change or influence the local vascular endothelium, making the endothelium more 'sticky' through the presence of compounds called adhesion molecules, and increasing the expression of procoagulant molecules. Changes in the condition of the vascular endothelium increase clotting in local blood vesselsto toareas helpofstop bleeding andwith to inhibit the spread of bacteria.Leucocytes migrate inflammation, neutrophils arrivingnormally first, followed by monocytes and lymphocytes withinblood hours toflow. days. Leucocytes circulate in blood vessels following laminar Leucocytes make intermittent contact with the endothelium, roll along the vasculature for a while, and then detach and circulate in the center of the blood vessel as leucocytes before, if there is no further stimulation of adherent molecules. Ifrolling encounter inflamed endothelium which expresses activated integrin adhesion molecules, integrins mediate the formation of adhesions between leukocytes and the endothelium in theendothelial form oftight binding. Leucocytes can then migrate through narrow gaps assisted byreach the presence of other pairs of adhesion molecules (diapedesis). Leucocytes the location ofmediators damagedthat tissuechemotaxis(directional cell migration). Chemotactic attract the attention of neutrophils include anaphylatoxins, leukotrienes, chemokines such as IL-8 (produced macrophages) and bacterial products, especially formyl peptides. by The main physiological events during inflammation include: 1. Immediate vasoconstriction occurs in the local area 2. There is an increase in blood flow to the site of inflammation (vasodilation) 3.(leukocytes There is acan decrease in the and velocity flowvessel to the endothelium site of inflammation flow slowly stickoftoblood the blood 4.to There is anvessel increase in blood vessel endothelial adhesion (leukocytes can bind the blood endothelium) 5. There is an increase in vascular permeability (fluid enters the tissue) 6. Phagocytes enter tissue (through increased margination and extravasation) In a shortoftime after trauma or infection, blood vessels carry blood, resulting in flooding the capillary network. Therefore the tissue becomes red and hot. Increased capillary permeabilitytissue. resultsThe in the entry of fluid and(exudate) cells from the capillaries into the surrounding accumulated fluid has a higher protein content than normal fluid. This fluid accumulation causes swelling (edema).