Macrophage signaling and respiratory burst.

摘要: Macrophages are key defenders of the lung and play an essential role in mediating inflammatory response. Critical to this is activation NADPH oxidase. Through receptor-mediated interactions, extracellular stimuli activate pathways that signal for phosphorylation assembly Once oxidase activated, it produces superoxide H2O2 a process known as respiratory burst. The involvement O2.- antimicrobicidal function macrophages has been assumed many years, but now clear produced by burst functions second messenger activates major signaling alveolar macrophage. Both nuclear factor-kappaB activator protein-1 transcription factors activated burst, and, since these control inducible expression genes whose products part response, may be critical link between other responses. c-Jun N-terminal kinase (JNK) extracellular-regulated (ERK) pathways, two members mitogen-activated protein family, also JNK both exogenous endogenously H2O2. Studies with ERK have shown specific agonists not bolus H2O2, can pathway. pathway modulates via factor Elk-1 controls production c-Fos factor. Although understanding mechanism redox its infancy, becoming reactive oxygen species profound effect on intracellular ultimately modulating gene expression.