ArticleCell communication and signaling : CCS2025
High-fat diet impairs microbial metabolite production and aggravates influenza A infection.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Dietary Bacillus sp. Modulates Multi-tissue Metabolism Through Gut Microbiota Remodeling in High-fat Fed Larimichthys crocea.Probiotics and antimicrobial proteins · 2026Article
- Gut Microbiota and Probiotics in Influenza: A Narrative Review of Mechanisms and Emerging Evidence.Viruses · 2026Review
- Cellular senescence dysregulates antiviral interferon responses in idiopathic pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Role and Mechanisms of Gut Microbiota in Infectious Diseases: Recent Evidence from Animal Models.Biology · 2026Review
- Effects of metabolic syndrome on pulmonary infection in pediatric bronchial asthma: a narrative review.Frontiers in pediatrics · 2026Review
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Authors and funding
11 authors.
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Abstract
backgroundAlterations in the gut microbiom can significantly impact various regions in the human body, including the pulmonary tract. This study investigates alterations in the gut microbiome during a high-fat diet (HFD), particularly short-chain fatty acids (SCFAs), and how these metabolites affect lung infection caused by Influenza A virus (IAV).
methodsWe used a HFD-mouse model to evaluate gut microbiota composition, SCFA levels, and pulmonary outcomes following IAV infection. Microbial changes were analyzed via taxonomic and functional profiling and SCFA levels were measured from non-obese and obese serum donors. Ultimately, acetate's effects were tested ex vivo in human precision-cut lung slices (PCLS) and in vitro in pulmonary epithelial cells. Mechanistic studies investigated the involvement of the SCFA receptor free fatty acid receptor 2 (FFAR2) and intracellular antiviral pathways.
resultsOur data indicates an increased Firmicutes/Bacteroidetes ratio of the gut microbiome and an altered carbohydrate metabolism, leading to reduced SCFA production. Infected HFD mice showed increased IAV titers and sustained microbial alterations. Interestingly, acetate demonstrated antiviral effects in both the human PCLS model and pulmonary cells with an reduced viral replication. These effects depended on FFAR2, which also acts as an IAV co-receptor, as acetate treatment led to FFAR2 internalization and influenced host cell metabolism in our in vitro data.
conclusionHFD alters the SCFA production, reducing acetate levels in the gut microbiome. This reduction may lead to higher viral loads and worsened disease in HFD mice infected with IAV. Our findings indicate that acetate has antiviral effects during IAV infection in both a human ex vivo lung model and pulmonary epithelial cells. Here, acetate prevents viral entry and affects the cellular metabolic state and antiviral response. Understanding these mechanisms could provide new targets for preventing and treating viral infections in individuals with diet-related health issues.
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