芳香烃受体
肠道菌群
新陈代谢
臭氧
肠粘膜
肠上皮
化学
生物
色氨酸
肠-脑轴
细胞生物学
微生物学
势垒函数
平衡
生物化学
毒性
受体
结构完整性
犬尿氨酸
微生物代谢
作者
Jiahao Zhang,Miao Li,Yuzhi Guo,Xinhang Jiang,Wenxue Li,Jingwen Huang,Yahan Yang,Zehua Ou,Yulu Cai,Yue Kong,Lian Li,Bo Deng,Lizhu Ye,Liping Chen,Qing Wang,Daochuan Li,Wen Chen,Shen Chen
标识
DOI:10.1016/j.envint.2026.110128
摘要
The increasing frequency of heat waves, combined with elevating ozone levels, constitutes an increasingly significant threat to public health. In this study, 8-week-old male C57BL/6J mice were subjected to individual or combined exposure of ozone (1 ppm) and heat (34°C) for 4 weeks. Both ozone and heat exposure disrupted intestinal barrier integrity and intestinal stem cell (ISC) function, with the most severe effects observed under combined exposure. Notably, co-exposure to ozone and heat resulted in the largest increase in Alistipes finegoldii (A. finegoldii) abundance, accompanied by enhanced tryptophan metabolism activity. Gut microbiota depletion and vertical microbiota transfer, together with intestinal content gavage, demonstrated the critical role of gut microbiota and their metabolites in mediating intestinal disruption. Colonization by A. finegoldii impaired ISC proliferation and differentiation, with elevated levels of indole and its derivatives, including indole-3-acetic acid (IAA) and tryptamine. Moreover, inhibition of aryl hydrocarbon receptor (AhR) signaling alleviated co-exposure-induced of intestinal injury. Mechanistically, AhR activation contributed to mitochondrial dysfunction. Interaction analysis indicated that ozone and heat primarily acted in an additive manner on gut integrity and microbiota dysbiosis. This study reveals that the A. finegoldii-tryptophan catabolite-AhR axis mediates the disruption of intestinal homeostasis induced by combined ozone and heat exposure.
科研通智能强力驱动
Strongly Powered by AbleSci AI