炎症是抵抗外界病原体入侵及组织损伤的一道重要的防御机制。但当机体处于持续性的炎症状态时，过多的中性粒细胞聚集，可进一步造成自身组织的损伤，导致炎症相关性疾病的发生。胆碱能抗炎通路（cholinergic anti‑inflammatory pathway, CAP）将神经系统和免疫系统紧密地联系在一起，刺激迷走神经可通过释放乙酰胆碱（acetylcholine, ACh）作用于免疫细胞表面的胆碱能受体，减少促炎细胞因子的释放，从而减轻炎症反应，有利于组织的修复。急性呼吸窘迫综合征（acute respiratory distress syndrome, ARDS）是一种高致残甚至致命的临床综合征。病理学表现为急性、弥漫性的炎症性肺损伤。减轻ARDS患者的肺损伤仍是近年来研究的一个热点。文章就CAP在不同模型诱导的ARDS中的作用及其可能的机制进行综述。
Inflammation is an important defense mechanism against external pathogen invasion and tissue damage. However, when the body is in a persistent inflammatory state, excessive accumulation of neutrophils may cause further severely tissue damage, leading to inflammation‑related diseases. The cholinergic anti‑inflammatory pathway (CAP) links the nervous system and the immune system closely together. Stimulation of the vagus nerve can release acetylcholine (ACh) which then binds to cholinergic receptors on the surface of immune cells and suppress the release of pro‑inflammatory cytokines, so as to reduce inflammatory response and facilitate tissue recovery. Acute respiratory distress syndrome (ARDS) is a highly disabling and even fatal clinical syndrome. The pathological manifestations are acute and diffuse inflammatory lung injury. Reducing lung injury in ARDS patients is still a hot topic in recent years. This review summarized the role of CAP in ARDS induced by different models and its possible mechanisms.
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