Clostridium butyricum-induced ω-3 fatty acid 18-HEPE elicits anti-influenza virus pneumonia effects through interferon-λ upregulation
Ontology highlight
ABSTRACT: 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.
INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase
SUBMITTER: Tadashi Ariyoshi
PROVIDER: MTBLS4590 | MetaboLights | 2023-05-30
REPOSITORIES: MetaboLights
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MTBLS4590 | Other | |||
| FILES | Other | |||
| a_MTBLS4590_LC-MS_negative_reverse-phase_metabolite_profiling.txt | Txt | |||
| files-all.json | Other | |||
| i_Investigation.txt | Txt |
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