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Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice
Open accessAbstract
BACKGROUND: The constitutive inflammation that characterizes advanced age is termed inflamm-aging. This process is associated with age-related changes to immune homeostasis and gut microbiota. We investigated the relationship between aging and gut microbiota lipopolysaccharide (LPS)-inducible inflammation. RESULTS: A taxonomy-based analysis showed that aging resulted in increased prevalence of the phyla Firmicutes and Actinobacteria and a reduced prevalence of Bacteroidetes and Tenericutes, resulting in an increase in the Firmicutes to Bacteroidetes ratio. The levels of plasmatic and fecal lipopolysaccharides were higher in aged mice. Aging induced the expression of p16 and the activation of nuclear factor-kappa B (NF-κB) in the colon of aged mice. Interestingly, the expression level of sterile α-motif domain- and HD domain-containing protein 1 (SAMHD1) in the colon was higher in aged mice than in young mice, while cyclin-dependent kinase-2 and cyclin E levels were lower in aged mice than in young mice. The lipopolysaccharide fraction of fecal lysates (LFL) from young or aged mice increased p16 and SAMHD1 expression and NF-κB activation in peritoneal macrophages from wild-type mice, in a TLR4-dependent manner. However, LFLs did not induce NF-κB activation and SAMHD1 expression in peritoneal macrophages from TLR4-deificent mice, whereas they significantly induced p16 expression. Nevertheless, p16 expression was induced more potently in macrophages from WT mice than in macrophages from TLR4-deficient mice. CONCLUSION: Aging increased p16 and SAMHD1 expression, gut microbiota LPS production, and NF-κB activation; thereby, signifying that gut microbiota LPS may accelerate inflamm-aging and SAMHD1 may be an inflamm-aging marker.
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“Geriatric mice have been shown to have increased gut permeability which results in bacterial lipopolysaccharide (LPS) leakage into the blood stream and activation of mononuclear phagocytes via binding to Toll-like receptor (TLR)4 (28,29).”
From The impact of ageing on monocytes and macrophages (2021) · cites this paper as [29]
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Metadata
- Authors
- Kim, K.-A., Jeong, J.-J., Yoo, S.-Y., & Kim, D.-H.
- Affiliations
- Kyung Hee University (KR)
- Corresponding author
- Kim, Dong-Hyun
- Venue
- BMC Microbiology
- Published
- 2016-01-16
- Volume
- 16
- Issue
- 1
- Pages
- 9-9
- ISSN
- 1471-2180 (ISSN-L)
- PMC
- PMC4715324
- OpenAlex
- W2248565900
- Cited by
- 196
- References
- 35
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 36 · 2023: 26 · 2022: 27 · 2021: 18 · 2020: 18 · 2019: 14 · 2018: 11 · 2017: 14 · 2016: 8
- FWCI
- 8.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- BMC Microbiology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Research Foundation (2013M3A9B6076413)
- Ministry of Science, ICT and Future Planning (2013M3A9B6076413)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- inflammaging, gut microbiota, lipopolysaccharide, aging, SAMHD1, p16, NF-κB activation, TLR4, peritoneal macrophages, Firmicutes/Bacteroidetes ratio, CDK2, cyclin E, age-related inflammation
- MeSH terms
- Gastrointestinal Microbiome, Aging, Animals, Bacteria, Humans, Inflammation, Lipopolysaccharides, Male, Mice, Inbred C57BL, Tumor Necrosis Factor-alpha, NF-kappa B, Gastrointestinal Tract, Toll-Like Receptor 4, Mice
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