' Host Tissues
Kinin System Clotting/ ^a Arachidonic Acid Fibrinolytic C5a" Systems
Bradykinin Mi Prostaglandins
Fig. 1 Effector mechanisms of the innate immune response. Innate immune recognition of pathogen associated molecular patterns (PAMPs) such as the Gram negative bacterial wall constituent, lipopolysaccharide (LPS), activates multiple host mediator systems that promote inflammation and the generation of antimicrobial agents. Activation of Factor XII (Hageman Factor) leads to the induction of kallikrein kinin, clotting, and fibrinolytic systems as well as the activation of complement. Activation of these systems results in the generation of ana phylotoxins, including bradykinin and complement cleavage products (e.g., C3a, C5a, C5b 9), which are highly proinflam matory. Priming and activation of macrophages and neutrophils enhance their release of proteases, toxic oxygen radicals, and proinflammatory cytokines (e.g., interleukin 1b (IL 1b) and tumor necrosis factor a (TNF a)). Host tissue activation leads to the production of platelet activating factor (PAF), nitric oxide (NO), and lipid derived mediators of inflammation (e.g., prostaglandins, leukotrienes, and thromboxanes). Host innate recognition of invasive pathogens stimulates an acute phase re sponse characterized by increased hepatic synthesis of proteins involved in both detection and clearance of infectious agents, including serum amyloid proteins (SAP), LPS binding protein (LBP), and C reactive protein (CRP).
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