Impact of aging on gut-lung-adipose tissue interactions and lipid metabolism during influenza infection in mice
Bogard G., Makki K., Brito-Rodrigues P., Tan J., Molendi-Coste O., Barthelemy J.
Animal Study, published in Sci Rep (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Sci Rep (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41145556
- PMCID
- PMC12559434
- DOI
- 10.1038/s41598-025-21363-1
- Citations
- 3
Abstract (original English)
Influenza remains a major threat to human health, especially for the elderly. Aging leads to substantial changes to lung function, gut microbiota, and white adipose tissue (WAT)-a key endocrine organ regulating energy balance and lipid metabolism. In the current study, we performed a multi-omics analysis to investigate how influenza impacts the gut-lung-adipose tissue axis differently with age at days 2, 4, 7, 14, and 28 post-infection (dpi). Compared to young-adult mice, aged mice experienced worse disease outcomes following infection, along with distinct WAT alterations, including impaired browning, heightened inflammation, and reduced innate immune cell recruitment. Age-related differences were also evidenced in infection-driven shifts in gut microbiota. Akkermansia levels rose only in young mice from 4 dpi, while Faecalibaculum and Muribaculum expanded exclusively in aged mice at 7 dpi, the only timepoint at which their abundance correlated with lung pathology. Serum metabolomics at 7 dpi also revealed age-dependent metabolic responses to infection. Compared to their non-infected counterparts, young mice had lower levels of p-Cresol-sulfate and Indoxyl-sulfate alongside higher triglycerides, whereas aged mice showed disrupted glycerophospholipid metabolism. By pinpointing specific gut bacteria as potential probiotics and identifying lipid pathways associated with disease pr
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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