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Publication : Clostridium butyricum-induced ω-3 fatty acid 18-HEPE elicits anti-influenza virus pneumonia effects through interferon-λ upregulation.

First Author  Hagihara M Year  2022
Journal  Cell Rep Volume  41
Issue  11 Pages  111755
PubMed ID  36516771 Mgi Jnum  J:334658
Mgi Id  MGI:7424702 Doi  10.1016/j.celrep.2022.111755
Citation  Hagihara M, et al. (2022) Clostridium butyricum-induced omega-3 fatty acid 18-HEPE elicits anti-influenza virus pneumonia effects through interferon-lambda upregulation. Cell Rep 41(11):111755
abstractText  The precise mechanism by which butyrate-producing bacteria in the gut contribute to resistance to respiratory viral infections remains to be elucidated. Here, we describe a gut-lung axis mechanism and report that orally administered Clostridium butyricum (CB) enhances influenza virus infection resistance through upregulation of interferon (IFN)-lambda in lung epithelial cells. Gut microbiome-induced omega-3 fatty acid 18-hydroxy eicosapentaenoic acid (18-HEPE) promotes IFN-lambda production through the G protein-coupled receptor (GPR)120 and IFN regulatory factor (IRF)-1/-7 activations. CB promotes 18-HEPE production in the gut and enhances omega-3 fatty acid sensitivity in the lungs by promoting GPR120 expression. This study finds a gut-lung axis mechanism and provides insights into the treatments and prophylaxis for viral respiratory infections.
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