Clostridium butyricum-induced ω-3 fatty acid 18-HEPE elicits anti-influenza virus pneumonia effects through interferon-λ upregulation 2022 Hagihara

Highlights

• Oral administration of Clostridium butyricum attenuates influenza virus pneumonia
• Clostridium butyricum-induced IFN-λ can enhance influenza virus infection resistance
• Orally administered Clostridium butyricum enhances 18-HEPE production in the gut
• 18-HEPE upregulates IFN-λ in lungs through GPR120 and IRF-1/-7 activation

Summary

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)-λ in lung epithelial cells. Gut microbiome-induced ω-3 fatty acid 18-hydroxy eicosapentaenoic acid (18-HEPE) promotes IFN-λ 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 ω-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.

Open access, https://www.cell.com/cell-reports/fulltext/S2211-1247(22)01638-2