Interaction between intestinal mycobiota and microbiota shapes lung inflammation
Youxia Wang,
Fang He,
Bingnan Liu,
Xiaoyan Wu,
Ziyi Han,
Xuefei Wang,
Yuexia Liao,
Jielin Duan,
Wenkai Ren
Affiliations
Youxia Wang
State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science South China Agricultural University Guangzhou China
Fang He
College of Veterinary Medicine Southwest University Chongqing China
Bingnan Liu
State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science South China Agricultural University Guangzhou China
Xiaoyan Wu
State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science South China Agricultural University Guangzhou China
Ziyi Han
State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science South China Agricultural University Guangzhou China
Xuefei Wang
School of Basic Medical Sciences Capital Medical University Beijing China
Yuexia Liao
School of Nursing & School of Public Health Yangzhou University Yangzhou China
Jielin Duan
Department of Allergy and Clinical Immunology, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health The First Affiliated Hospital of Guangzhou Medical University Guangzhou China
Wenkai Ren
State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science South China Agricultural University Guangzhou China
Abstract 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 Escherichia coli (E. coli) overgrowth and translocation to the lung during infection, which induced lung accumulation of the CD45+F4/80+Ly6G−Ly6C−CD11b+CD11c+ 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.
