期刊
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
卷 39, 期 2, 页码 127-132出版社
AMER THORACIC SOC
DOI: 10.1165/rcmb.2008-0091TR
关键词
phagocytes; host defense; G protein-coupled receptors; protein kinase A; exchange protein activated by cyclic AMP
资金
- NHLBI NIH HHS [K08 HL078727, K08 HL078727-05, HL058897, HL078727] Funding Source: Medline
Cyclic adenosine monophosphate (CAMP) was the original second messenger to be discovered. Its formation is promoted by adenylyl cyclase activation after ligation of G protein-coupled receptors by ligands including hormones, autocoids, Prostaglandins, and pharmacologic agents. Increases in intracellular cAMP generally suppress innate immune functions, including inflammatory mediator generation and the phagocytosis and killing of microbes. The importance of the host CAMP axis in regulating antimicrobial defense is underscored by the fact that microbes have evolved virulence-enhancing strategies that exploit it. Many clinical situations that predispose to infection are associated with increases in CAMP, and therapeutic strategies to interrupt cAMP generation or actions have immunostimulatory potential. This article reviews the anatomy of the CAMP axis, the mechanisms by which it controls phagocyte immune function, microbial strategies to dysregulate it, and its clinical relevance.
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