Human gut bacteria produce ΤΗ17-modulating bile acid metabolites View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2022-03-16

AUTHORS

Donggi Paik, Lina Yao, Yancong Zhang, Sena Bae, Gabriel D. D’Agostino, Minghao Zhang, Eunha Kim, Eric A. Franzosa, Julian Avila-Pacheco, Jordan E. Bisanz, Christopher K. Rakowski, Hera Vlamakis, Ramnik J. Xavier, Peter J. Turnbaugh, Randy S. Longman, Michael R. Krout, Clary B. Clish, Fraydoon Rastinejad, Curtis Huttenhower, Jun R. Huh, A. Sloan Devlin

ABSTRACT

The microbiota modulates gut immune homeostasis. Bacteria influence the development and function of host immune cells, including T helper cells expressing interleukin-17A (TH17 cells). We previously reported that the bile acid metabolite 3-oxolithocholic acid (3-oxoLCA) inhibits TH17 cell differentiation1. Although it was suggested that gut-residing bacteria produce 3-oxoLCA, the identity of such bacteria was unknown, and it was unclear whether 3-oxoLCA and other immunomodulatory bile acids are associated with inflammatory pathologies in humans. Here we identify human gut bacteria and corresponding enzymes that convert the secondary bile acid lithocholic acid into 3-oxoLCA as well as the abundant gut metabolite isolithocholic acid (isoLCA). Similar to 3-oxoLCA, isoLCA suppressed TH17 cell differentiation by inhibiting retinoic acid receptor-related orphan nuclear receptor-γt, a key TH17-cell-promoting transcription factor. The levels of both 3-oxoLCA and isoLCA and the 3α-hydroxysteroid dehydrogenase genes that are required for their biosynthesis were significantly reduced in patients with inflammatory bowel disease. Moreover, the levels of these bile acids were inversely correlated with the expression of TH17-cell-associated genes. Overall, our data suggest that bacterially produced bile acids inhibit TH17 cell function, an activity that may be relevant to the pathophysiology of inflammatory disorders such as inflammatory bowel disease. More... »

PAGES

907-912

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  • Journal

    TITLE

    Nature

    ISSUE

    7903

    VOLUME

    603

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41586-022-04480-z

    DOI

    http://dx.doi.org/10.1038/s41586-022-04480-z

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1146308429

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/35296854


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