Host Cell Responses

Following PRR recognition of its cognate PAMP, cellular activation of effector cells of the innate immune system, including neutrophils and macrophages, often leads to the generation of an inflammatory response that is elicited, in part, by cytokine production.[5] Proinflammatory cytokines, such as TNF-a and IL-1 p, are potent inducers of the acute-phase response, fever, and vascular endothelial activation. This latter event of endothelial activation in combination with PRR-mediated generation of the chemo-attractant IL-8, facilitates neutrophil recruitment to the site of infection. Upregulation of other cytokines, such as IL-6 and IL-12, following PRR activation contributes to the adaptive immune response by stimulating lymphocyte proliferation and differentiation.

In addition to cytokines, PRR-mediated cell activation elicits cellular production of toxic oxygen radicals and proteases (which have direct bactericidal effects), as well as the generation of lipid mediators of inflammation, including platelet-activating factor (PAF) and the arachidonic acid metabolites, prostaglandins, leuko-trienes, and thromboxanes.[5,6] Cell activation can further result in the release of antimicrobial peptides, including the well-characterized defensins and larger antimicrobial



Cytokines ^ Proteases


T Acute Phase | Hepatic Synthesis Macrophage

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