Evidence map›Paper›PMID 41387757›Full record

ArticleScientific reports2025

Streptococcus gordonii type VII secretion system substrate EsxA induces neutrophil extracellular trap formation in infective endocarditis.

Chih-Chieh Hsu, Yu-Chung Chuang, Ron-Bin Hsu, Jeng-Wei Chen, Jean-San Chia, Yi-Hsien Shih, Yu-Min Kuo, Chiau-Jing Jung

Abstract read
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In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Chih-Chieh HsuDepartment of Microbiology, Soochow University, Taipei, Taiwan.
Yu-Chung ChuangDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Ron-Bin HsuDepartment of Surgery, Division of Cardiovascular Surgery, College of Medicine, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan.
Jeng-Wei ChenDepartment of Surgery, Division of Cardiovascular Surgery, College of Medicine, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan.
Jean-San ChiaGraduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Yi-Hsien ShihDepartment of Dermatology, Taipei Medical University-Shuang Ho Hospital, New Taipei City, Taiwan.
Yu-Min KuoGraduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chiau-Jing JungDepartment of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, No. 250, Wuxing Street, Taipei, 11031, Taiwan. cjjung@tmu.edu.tw.

Funding

National Science and Technology Council NSTC112-2320-B-038-055-MY3National Science and Technology Council NSTC114-2320-B-031-002National Taiwan University Hospital 113-TMU122National Taiwan University Hospital 113-TMU123Taipei Medical University 113-TMU121
6 · The paper itself

Abstract

Type VII secretion system (T7SS) substrate EsxA contributes to the pathogenesis of several Gram-positive bacteria, but its role in viridans streptococci-induced infective endocarditis (IE) remains unclear. Genomic analysis of the Streptococcus gordonii DL1 strain identified a genetic locus encoding five T7SSb core machinery proteins (EsaA, EssA, EsaB, EssB, and EssC) and one substrate, EsxA. T7SSb mediates EsxA secretion, as evidenced by reduced secretion in the essC-deleted mutant and restoration upon complementation. In a rat model of IE, the esxA-deficient strain shows lower survival in circulation and reduced formation of vegetation, suggesting a role for EsxA in IE pathogenesis. Using a transwell system, molecules secreted from wild-type S. gordonii DL1 can induce the release of neutrophil extracellular traps (NETs) by neutrophils, and this activity is lost in the esxA-deficient strain. In addition, recombinant EsxA can dose-dependently induce NET formation, confirming a role for secreted EsxA in the induction of NET formation. Consistently, reduced and restored NET formation is observed in vivo in vegetations caused by esxA-deficient and complemented strains, respectively. Together, these data indicate that EsxA secretion mediated by T7SSb induces NET formation that contributes to bacterial survival in the circulation and vegetation formation in S. gordonii-induced IE.

Indexed as

Bacterial ProteinsEndocarditisEndocarditis, BacterialExtracellular TrapsNeutrophilsStreptococcal InfectionsStreptococcus gordoniiType VII Secretion SystemsAnimalsDisease Models, AnimalHumansRatsBacterial ProteinsType VII Secretion SystemsEsxAInfective endocarditisNeutrophil extracellular trapsStreptococcus gordoniiType VII secretion system

Identifiers

PMID41387757
PMCPMC12701049

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.