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The term "inflammatory response mediator" refers collectively to various endogenous chemical agents released during tissue injury or infection that regulate the initiation, amplification, and resolution phases of inflammation. These include cell-derived substances like cytokines, histamine, leukotrienes, and prostaglandins—produced locally at sites of injury—as well as plasma-derived factors such as complement proteins and kinins activated systemically from precursor forms in circulation. Each type plays distinct roles in modulating vascular changes (vasodilation/permeability), recruiting immune cells via chemotaxis, inducing pain/fever responses through nerve stimulation or pyrogenic effects, promoting pathogen clearance via phagocytosis/opsonization/cell lysis mechanisms—and ultimately facilitating tissue repair once harmful stimuli are eliminated. Because this designation encompasses numerous structurally unrelated molecules across several biochemical families—rather than one defined protein/receptor/enzyme—it cannot be considered a canonical therapeutic target itself.
Varies by drug class: - Enzyme inhibition (e.g., COX inhibitors reduce prostaglandin production). - Receptor antagonism/blockade (e.g., antihistamines). - Neutralization/blockade of cytokines or their receptors.
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