内源性大麻素系统(ECS),最初确定它在维持体内平衡方面的作用,特别是在调节大脑功能方面,已经演变成一个复杂的协调器,影响各种生理过程,超出其与神经系统的原始关联。值得注意的是,越来越多的证据强调了ECS在调节免疫反应中的关键作用。虽然ECS在细菌感染中的具体作用仍在研究中,令人信服的迹象表明其积极参与宿主-病原体相互作用。将ECS纳入细菌病原体感染的框架为我们对其功能的理解引入了一层复杂性。虽然一些研究提出了大麻素调节细菌功能和免疫反应的潜力,结果本身取决于所考虑的特定感染和大麻素.此外,ECS和肠道微生物群之间的双向关系强调了不同生理过程之间复杂的相互作用。ECS的影响力远远超出了它最初的发现,在一系列医疗条件下成为有希望的治疗目标,包括细菌感染,生态失调,还有败血症.这篇综述全面探讨了ECS在细菌调节中的复杂作用,宿主对细菌感染的反应,和微生物组的动态。特别强调大麻素受体类型1和2的作用,其信号传导复杂地影响微生物-宿主相互作用中的免疫细胞功能。
The endocannabinoid system (ECS), initially identified for its role in maintaining homeostasis, particularly in regulating brain function, has evolved into a complex orchestrator influencing various physiological processes beyond its original association with the nervous system. Notably, an expanding body of evidence emphasizes the ECS\'s crucial involvement in regulating immune responses. While the specific role of the ECS in bacterial infections remains under ongoing investigation, compelling indications suggest its active participation in host-pathogen interactions. Incorporating the ECS into the framework of bacterial pathogen infections introduces a layer of complexity to our understanding of its functions. While some studies propose the potential of cannabinoids to modulate bacterial function and immune responses, the outcomes inherently hinge on the specific infection and cannabinoid under consideration. Moreover, the bidirectional relationship between the ECS and the gut microbiota underscores the intricate interplay among diverse physiological processes. The ECS extends its influence far beyond its initial discovery, emerging as a promising therapeutic target across a spectrum of medical conditions, encompassing bacterial infections, dysbiosis, and sepsis. This review comprehensively explores the complex roles of the ECS in the modulation of bacteria, the host\'s response to bacterial infections, and the dynamics of the microbiome. Special emphasis is placed on the roles of cannabinoid receptor types 1 and 2, whose signaling intricately influences immune cell function in microbe-host interactions.