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.

中文翻译：

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Cyclic AMP：先天免疫细胞功能的主要调节器。

环磷酸腺苷 (cAMP) 是最初被发现的“第二信使”。在 G 蛋白偶联受体被配体（包括激素、autocoids、前列腺素和药物制剂）连接后，腺苷酸环化酶激活促进其形成。细胞内 cAMP 的增加通常会抑制先天免疫功能，包括炎症介质的产生以及微生物的吞噬和杀死。微生物已经进化出利用它的毒力增强策略这一事实强调了宿主 cAMP 轴在调节抗菌防御中的重要性。许多易于感染的临床情况与 cAMP 的增加有关，中断 cAMP 生成或作用的治疗策略具有免疫刺激潜力。