Evidence map›Paper›PMID 39792643›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense.

Peng Gu, Rongjuan Wei, Ruofan Liu, Qin Yang, Yuxuan He, Jianbin Guan, Wenhao He, Jiaxin Li, Yunfei Zhao, Li Xie and 11 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Trial
  2. Indole-3-carboxaldehyde fromGut microbes · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  9. Review
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

21 authors.

Peng GuDepartment of Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Rongjuan WeiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Ruofan LiuDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Qin YangDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Yuxuan HeDepartment of Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Jianbin GuanDepartment of Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Wenhao HeDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Jiaxin LiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Yunfei ZhaoDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Li XieDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Jie HeDepartment of Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Qingling GuoDepartment of Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Jiajia HuDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Jingna BaoDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510510, China.
Wandang WangDepartment of Clinical Medicine Laboratory, Affiliated Xiaolan Hospital, Southern Medical University, Zhongshan, 528415, China.
Jiayin GuoNMPA Key Laboratory for Research and Evaluation of Drug Metabolism, Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
Zhenhua ZengDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510510, China.
Zhongqing ChenDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510510, China.
Yong JiangDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.ORCID https://orcid.org/0000-0002-8087-5717
Zhanguo LiuDepartment of Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Peng ChenDepartment of Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.ORCID https://orcid.org/0000-0003-0473-205X

Funding

Guang Dong Basic and Applied Basic Research Foundation 2022A1515110070Guang Dong Basic and Applied Basic Research Foundation 2022B1515120024National Key R&D Program of China 2022YFA0806400National Natural Science Foundation of China 32071124National Natural Science Foundation of China 32271230National Natural Science Foundation of China 81971859National Natural Science Foundation of China 82130063National Natural Science Foundation of China 82241061
6 · The paper itself

Abstract

Older individuals experience increased susceptibility and mortality to bacterial infections, but the underlying etiology remains unclear. Herein, it is shown that aging-associated reduction of commensal Parabacteroides goldsteinii (P. goldsteinii) in both aged mice and humans critically contributes to worse outcomes of bacterial infection. The colonization of live P. goldsteinii conferred protection against aging-associated bacterial infections. Metabolomic profiling reveals a protective compound, apigenin, generated by P. goldsteinii, antagonizes bacterial clearance defects in aged mice. AMP-binding protein (ampB) is identified as a key gene involved in apigenin synthesis in P. goldsteinii using homologous recombination in bacteria. Mechanistically, apigenin binds directly to the potential sites on Fgr (M341 and D404), preventing its inhibitory role on Vav1 phosphorylation, and therefore promoting the activation of Cdc42/Rac1, Arp2/3 expression and subsequent actin reorganization, which contributes to the enhanced phagocytosis of macrophages to bacteria. Collectively, the findings suggest that dysbiosis of the gut microbiota may impair host defense mechanisms and increase susceptibility to bacterial infections in older adults and highlight the microbiota-apigenin-Fgr axis as a possible route to ameliorate aging-associated antibacterial defects.

Indexed as

AgingBacterial InfectionsDysbiosisGastrointestinal MicrobiomeAnimalsApigeninFemaleHumansMaleMiceMice, Inbred C57BLApigeninagingbacterial infectiongut microbiomemacrophage

Identifiers

PMID39792643
PMCPMC11948050

What OpenQuestion holds

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Registered trials

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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.