Wang Youxia, He Fang, Liu Bingnan, Wu Xiaoyan, Han Ziyi, Wang Xuefei, Liao Yuexia, Duan Jielin, Ren Wenkai
State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science South China Agricultural University Guangzhou China.
College of Veterinary Medicine Southwest University Chongqing China.
Imeta. 2024 Sep 14;3(5):e241. doi: 10.1002/imt2.241. eCollection 2024 Oct.
Gut microbiota is an intricate microbial community containing bacteria, fungi, viruses, archaea, and protozoa, and each of them contributes to diverse aspects of host health. Nevertheless, the influence of interaction among gut microbiota on host health remains uncovered. Here, we showed that the interaction between intestinal fungi and bacteria shaped lung inflammation during infection. Specifically, antifungal drug-induced dysbiosis of gut mycobiota enhanced lung inflammation during infection. Dysbiosis of gut mycobiota led to gut () overgrowth and translocation to the lung during infection, which induced lung accumulation of the CD45F4/80Ly6GLy6CCD11bCD11c macrophages. Clearance of macrophages or deletion of TLR4 (Toll-like receptor 4, recognition of LPS) rather than Dectin-1 (recognition of beta-1,3/1,6 glucans on fungi) blocked the antifungal drug-induced aggravation of lung inflammation during infection. These findings suggest that the interaction between intestinal mycobiota and commensal bacteria affects host health through the gut-lung axis, offering a potential therapeutic target for ameliorating lung inflammation during infection.
肠道微生物群是一个复杂的微生物群落，包含细菌、真菌、病毒、古细菌和原生动物，它们各自对宿主健康的多个方面都有贡献。然而，肠道微生物群之间的相互作用对宿主健康的影响仍未被揭示。在此，我们表明肠道真菌和细菌之间的相互作用在感染期间塑造了肺部炎症。具体而言，抗真菌药物诱导的肠道真菌群失调在感染期间加剧了肺部炎症。肠道真菌群失调导致感染期间肠道（）过度生长并转移至肺部，这诱导了CD45F4/80Ly6GLy6CCD11bCD11c巨噬细胞在肺部的聚集。清除巨噬细胞或敲除TLR4（Toll样受体4，识别LPS）而非Dectin-1（识别真菌上的β-1,3/1,6葡聚糖）可阻断抗真菌药物在感染期间诱导的肺部炎症加重。这些发现表明肠道真菌群与共生细菌之间的相互作用通过肠-肺轴影响宿主健康，为改善感染期间的肺部炎症提供了一个潜在的治疗靶点。
