Inflammation is the body's reaction to the invasion of an infectious agent, antigen challenge, physical, chemical or traumatic injury. Besides, a great quantity of distant events occurs during inflammation. These include: acute phase reactants and complement components (trough the liver) synthesis; fever caused by pyrogens that act on the hypothalamus; and systemic immunity, resulting this last one by activating lymphocytes in lymphoid peripheral tissues.
Due to its complex form and the great number of factors taking place in all the stages, inflammation is considered like a number of continuous events that overlap and not like a sequential process that follows step by step, in spite of all our efforts to define it and understand it as such.
The inflammatory process does not place by itself. This one presents complex interactions with other elements. Inflammation is a mechanism that is integrated and self-regulated, where pro-inflammatory substances are released and anti-inflammatory ones tend to balance them.
The mediators released during the inflammatory process perpetuate the inflammatory response and are responsible of the clinical signs that are associated to inflammation, including pain and fever. Inflammation mediators are created from cells as well as from fluids that reach the site of injury cell trough the blood. Leucocytes are a great source of a variety of chemical mediators during inflammation. These cells, as well as other cells that are injured and finally die, either initial injury or subsequent inflammation, perpetrate the inflammatory response.
A great variety of mediators have been identified. Great part of them shows slightly different effects, multiple functions and multiple interactions between each other. Almost of them are used during early stages and occasionally during last ones in the inflammatory process. Besides, all of them play an important and poorly defined role in the body's response facing a stimulus or offensive agents.
Many of these show some type of effect over vascular bed, increasing permeability. Many as well show effects on the white cells behaviour increased its motility, activating its metabolic processing or stimulating phagocytosis.
Mediators include: lysosomal enzymes and other types; granular mediators as histamine and serotonin; eicosanoids or products of the arachidonic acid (AA) metabolism, like prostaglandins, prostacyclin and thromboxanes; platelet activating factor (PAF); reactive oxygen intermediates (ROI); and cytokines such as tumour necrosis factor (TNF), inteleukin-1 (IL-1) and interleukin-6 (IL-6). The role that each of these mediator plays in the inflammatory response varies depending on part of the stage of the inflammation during the mediator is released.
The plasma mediators are important partners in the inflammatory process. The example include: kinins (e.g., bradykinin) released from its precursor forms, after adequately physiologic or pathologic stimulation; complement system and peptides derived from this, released after activation is done either by the classic pathway or the alternative pathway; fibrinopeptides are released during fibrinogen conversion to fibrin, during the coagulation process and eventually proteolysis of fibrin to plasmin.
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