Evidence map›Paper›PMID 26772806›Full record

ArticleBMC microbiology2016

Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice.

Kyung-Ah Kim, Jin-Ju Jeong, Sul-Young Yoo, Dong-Hyun Kim

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

122 citing papers in PubMed, 2 syntheses or guidelines pooled it, 190 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  7. Article
  8. The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026
    Review
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  19. Specific microbial ratio in the gut microbiome is associated with multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Review

62 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Kyung-Ah KimDepartment of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, 1, Hoegi, Dongdaemun-ku, Seoul, 130-701, Korea.
Jin-Ju JeongDepartment of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, 1, Hoegi, Dongdaemun-ku, Seoul, 130-701, Korea.
Sul-Young YooDepartment of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, 1, Hoegi, Dongdaemun-ku, Seoul, 130-701, Korea.
Dong-Hyun KimDepartment of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, 1, Hoegi, Dongdaemun-ku, Seoul, 130-701, Korea. dhkim@khu.ac.kr.
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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.

resultsA 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.

conclusionAging 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.

Indexed as

Gastrointestinal MicrobiomeAgingAnimalsBacteriaGastrointestinal TractHumansInflammationLipopolysaccharidesMaleMiceMice, Inbred C57BLNF-kappa BToll-Like Receptor 4Tumor Necrosis Factor-alphaLipopolysaccharidesNF-kappa BToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID26772806
PMCPMC4715324
OpenAlexW2248565900

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.