Evidence map›Paper›PMID 39909037›Full record

ArticleCell host & microbe2025

A human gut bacterium antagonizes neighboring bacteria by altering their protein-folding ability.

Bentley Lim, Jinghua Xu, Igor H Wierzbicki, Carlos G Gonzalez, Zhe Chen, David J Gonzalez, Xiang Gao, Andrew L Goodman

Abstract read
In one paragraph

Article in Cell host & microbe, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. An electron transport complex required in the gut sensitizesProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. A nonenzymatic effector disruptsProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
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

8 authors.

Bentley LimDepartment of Microbial Pathogenesis and Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06536, USA.
Jinghua XuState Key Laboratory of Microbial Technology, Shandong University, Qingdao 266237, China.
Igor H WierzbickiDepartment of Pharmacology and the Skaggs School of Pharmacy and Pharmaceutical Sciences, Center of Microbiome Innovation, University of California, San Diego, La Jolla, San Diego, CA 92093, USA.
Carlos G GonzalezDepartment of Pharmacology and the Skaggs School of Pharmacy and Pharmaceutical Sciences, Center of Microbiome Innovation, University of California, San Diego, La Jolla, San Diego, CA 92093, USA.
Zhe ChenState Key Laboratory of Microbial Technology, Shandong University, Qingdao 266237, China.
David J GonzalezDepartment of Pharmacology and the Skaggs School of Pharmacy and Pharmaceutical Sciences, Center of Microbiome Innovation, University of California, San Diego, La Jolla, San Diego, CA 92093, USA.
Xiang GaoState Key Laboratory of Microbial Technology, Shandong University, Qingdao 266237, China.
Andrew L GoodmanDepartment of Microbial Pathogenesis and Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06536, USA. Electronic address: andrew.goodman@yale.edu.

Funding

UCSD/SDSU IRACDAK12GM068524 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TREJO, JOANN · 2003 to 2025
$24.4M
Causes and consequences of interpersonal microbial variationR35GM118159 · NIGMS · YALE UNIVERSITY · PI Andrew L Goodman · 2016 to 2026
$5.6M
Diet transformation by the microbiome and its impact on bacterial infectionR01DK133798 · NIDDK · YALE UNIVERSITY · PI Jorge E Galan, Andrew L Goodman · 2022 to 2026
$4.1M
Microbiome Driven Proteolysis as a Contributing Factor to Severity of Ulcerative Colitis Disease ActivityR01DK131005 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GONZALEZ, DAVID J · 2022 to 2024
$1.6M
NIDDK NIH HHS R01 DK131005NIDDK NIH HHS R01 DK133798NIGMS NIH HHS K12 GM068524NIGMS NIH HHS R35 GM118159
6 · The paper itself

Abstract

Antagonistic interactions play a key role in determining microbial community dynamics. Here, we report that one of the most widespread contact-dependent effectors in human gut microbiomes, Bte1, directly targets the PpiD-YfgM periplasmic chaperone complex in related microbes. Structural, biochemical, and genetic characterization of this interaction reveals that Bte1 reverses the activity of the chaperone complex, promoting substrate aggregation and toxicity. Using Bacteroides, we show that Bte1 is active in the mammalian gut, conferring a fitness advantage to expressing strains. Recipient cells targeted by Bte1 exhibit sensitivity to membrane-compromising conditions, and human gut microbes can use this effector to exploit pathogen-induced inflammation in the gut. Further, Bte1 allelic variation in gut metagenomes provides evidence for an arms race between Bte1-encoding and immunity-encoding strains in humans. Together, these studies demonstrate that human gut microbes alter the protein-folding capacity of neighboring cells and suggest strategies for manipulating community dynamics.

Indexed as

Bacterial ProteinsBacteroidesGastrointestinal MicrobiomeProtein FoldingAnimalsGastrointestinal TractHumansMolecular ChaperonesBacterial ProteinsMolecular Chaperonesbacterial antagonismBacteroideschaperonegut microbiomepeptidyl-prolyl isomerase

Identifiers

PMID39909037
PMCPMC11931560

What OpenQuestion holds

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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.