美国阿尔伯特·爱因斯坦医学院Paul S. Frenette小组发现，肠道微生物组调节心理压力引起的炎症。这一研究成果在线发表于2020年7月30日的《免疫》。

在本研究中，利用镰状细胞病的血管闭塞性发作（VOE）作为血管疾病模型，研究人员发现压力可通过引起糖皮质激素的激素反应来增强VOE，这些激素反应可增强肠道壁的通透性，导致微生物依赖的白介素17A（IL-17A）固有层辅助性T细胞17（Th17）的分泌，随后引发VOE中性粒细胞循环池扩大。

研究人员确定分段丝状细菌是应激诱导衰老嗜中性粒细胞扩增所必需的，这增强了小鼠的VOE。重要的是，抑制糖皮质激素的合成、阻断IL-17A或诱导Th17细胞产生肠道菌群的耗竭显著降低了压力诱导的VOE。这些结果提供了潜在的治疗策略，以减弱心理压力对急性血管闭塞的影响。

据介绍，心理压力会对人类各种疾病（包括心血管系统疾病）产生不利影响。但是，压力影响疾病的机制尚不清楚。

附：英文原文

Title: The Gut Microbiome Regulates Psychological-Stress-Induced Inflammation

Author: Chunliang Xu, Sung Kyun Lee, Dachuan Zhang, Paul S. Frenette

Issue&Volume: 2020-07-30

Abstract: Psychological stress has adverse effects on various human diseases, including thoseof the cardiovascular system. However, the mechanisms by which stress influences diseaseactivity remain unclear. Here, using vaso-occlusive episodes (VOEs) of sickle celldisease as a vascular disease model, we show that stress promotes VOEs by elicitinga glucocorticoid hormonal response that augments gut permeability, leading to microbiota-dependentinterleukin-17A (IL-17A) secretion from T helper 17 (Th17) cells of the lamina propria,followed by the expansion of the circulating pool of aged neutrophils that triggerVOEs. We identify segmented filamentous bacteria as the commensal essential for thestress-induced expansion of aged neutrophils that enhance VOEs in mice. Importantly,the inhibition of glucocorticoids synthesis, blockade of IL-17A, or depletion of theTh17 cell-inducing gut microbiota markedly reduces stress-induced VOEs. These resultsoffer potential therapeutic targets to limit the impact of psychological stress on acute vascular occlusion.

DOI: 10.1016/j.immuni.2020.06.025

Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30280-6