Evidence map›Paper›PMID 37169880›Full record

ArticleNature cell biology2023

Bacterial induction of B cell senescence promotes age-related changes in the gut microbiota.

Shimpei Kawamoto, Ken Uemura, Nozomi Hori, Lena Takayasu, Yusuke Konishi, Kazutaka Katoh, Tomonori Matsumoto, Masae Suzuki, Yusuke Sakai, Tatsuyuki Matsudaira and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 70 citations in OpenAlex.

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  15. Molecular evolution of animal aging.The EMBO journal · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 1 country.

Shimpei Kawamoto *Department of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan. kshimpei@biken.osaka-u.ac.jp.ORCID http://orcid.org/0000-0002-7033-671X
Ken Uemura *Department of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Nozomi HoriDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Lena TakayasuRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Yusuke KonishiDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Kazutaka KatohDepartment of Genome Informatics, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Tomonori MatsumotoDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Masae SuzukiDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Yusuke SakaiNational Institute of Infectious Diseases, Tokyo, Japan.
Tatsuyuki MatsudairaDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.ORCID http://orcid.org/0000-0003-2271-5317
Takahiro AdachiMedical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Naoko OhtaniGraduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.ORCID http://orcid.org/0000-0001-8934-0797
Daron M StandleyDepartment of Genome Informatics, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Wataru SudaRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Shinji FukudaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan.ORCID http://orcid.org/0000-0001-5161-9880
Eiji HaraDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan. ehara@biken.osaka-u.ac.jp.ORCID http://orcid.org/0000-0001-7821-3960
The University of Osaka · JPRIKEN Center for Integrative Medical Sciences · JPNational Institute of Infectious Diseases · JPOsaka Metropolitan University · JPTokyo Medical and Dental University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The elucidation of the mechanisms of ageing and the identification of methods to control it have long been anticipated. Recently, two factors associated with ageing-the accumulation of senescent cells and the change in the composition of gut microbiota-have been shown to play key roles in ageing. However, little is known about how these phenomena occur and are related during ageing. Here we show that the persistent presence of commensal bacteria gradually induces cellular senescence in gut germinal centre B cells. Importantly, this reduces both the production and diversity of immunoglobulin A (IgA) antibodies that target gut bacteria, thereby changing the composition of gut microbiota in aged mice. These results have revealed the existence of IgA-mediated crosstalk between the gut microbiota and cellular senescence and thus extend our understanding of the mechanism of gut microbiota changes with age, opening up possibilities for their control.

Indexed as

Gastrointestinal MicrobiomeAnimalsBacteriaB-LymphocytesCellular SenescenceImmunoglobulin AMiceImmunoglobulin A

Identifiers

PMID37169880
OpenAlexW4376135071

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.