Gut microbiota modulates lung fibrosis severity following acute lung injury in mice

Ozioma S. Chioma, Elizabeth K. Mallott, Austin Chapman, Joseph C. Van Amburg, Hongmei Wu, Binal Shah-Gandhi, Nandita Dey, Marina E. Kirkland, M. Blanca Piazuelo, Joyce Johnson, Gordon R. Bernard, Sobha R. Bodduluri, Steven Davison, Bodduluri Haribabu, Seth R. Bordenstein, Wonder P. Drake

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Independent studies demonstrate the significance of gut microbiota on the pathogenesis of chronic lung diseases; yet little is known regarding the role of the gut microbiota in lung fibrosis progression. Here we show, using the bleomycin murine model to quantify lung fibrosis in C57BL/6 J mice housed in germ-free, animal biosafety level 1 (ABSL-1), or animal biosafety level 2 (ABSL-2) environments, that germ-free mice are protected from lung fibrosis, while ABSL-1 and ABSL-2 mice develop mild and severe lung fibrosis, respectively. Metagenomic analysis reveals no notable distinctions between ABSL-1 and ABSL-2 lung microbiota, whereas greater microbial diversity, with increased Bifidobacterium and Lactobacilli, is present in ABSL-1 compared to ABSL-2 gut microbiota. Flow cytometric analysis reveals enhanced IL-6/STAT3/IL-17A signaling in pulmonary CD4 + T cells of ABSL-2 mice. Fecal transplantation of ABSL-2 stool into germ-free mice recapitulated more severe fibrosis than transplantation of ABSL-1 stool. Lactobacilli supernatant reduces collagen 1 A production in IL-17A- and TGFβ1-stimulated human lung fibroblasts. These findings support a functional role of the gut microbiota in augmenting lung fibrosis severity.

Original languageEnglish
Article number1401
JournalCommunications Biology
Issue number1
StatePublished - Dec 2022


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