Evidence map›Paper›PMID 39052722›Full record

ArticleThe Journal of infectious diseases2024

Streptococcus suis Serotype 2 Type IV Secretion Effector SspA-1 Induces Proinflammatory Cytokine Production via TLR2 Endosomal and Type I Interferon Signaling.

Supeng Yin, Mengmeng Yuan, Sirui Zhang, Hongdan Chen, Jing Zhou, Tongyu He, Gang Li, Yanlan Yu, Fan Zhang, Ming Li and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of infectious diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

11 authors.

Supeng YinDepartment of Breast and Thyroid Surgery, Chongqing General Hospital, Chongqing, China.
Mengmeng YuanDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Sirui ZhangThe First Clinical Medical School, Guangzhou University of Chinese Medicine, Guangzhou, China.
Hongdan ChenDepartment of Breast and Thyroid Surgery, Chongqing General Hospital, Chongqing, China.
Jing ZhouDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Tongyu HeDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Gang LiDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Yanlan YuDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Fan ZhangDepartment of Breast and Thyroid Surgery, Chongqing General Hospital, Chongqing, China.
Ming LiDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Yan ZhaoDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.ORCID 0000-0002-3195-2405

Funding

National Natural Science Foundation of China 82002119Natural Science Foundation of Chongqing Municipality, China cstc2019jcyj-msxmX0142
6 · The paper itself

Abstract

The subtilisin-like protease-1 (SspA-1) plays an important role in the pathogenesis of a highly virulent strain of Streptococcus suis 2. However, the mechanism of SspA-1-triggered excessive inflammatory response is still unknown. In this study, we demonstrated that activation of type I IFN signaling is required for SspA-1-induced excessive proinflammatory cytokine production. Further experiments showed that the TLR2 endosomal pathway mediates SspA-1-induced type I IFN signaling and the inflammatory response. Finally, we mapped the major signaling components of the related pathway and found that the TIR adaptor proteins Mal, TRAM, and MyD88 and the downstream activation of IRF1 and IRF7 were involved in this pathway. These results explain the molecular mechanism by which SspA-1 triggers an excessive inflammatory response and reveal a novel effect of type I IFN in S. suis 2 infection, possibly providing further insights into the pathogenesis of this highly virulent S. suis 2 strain.

Indexed as

CytokinesEndosomesInterferon Type ISignal TransductionStreptococcus suisToll-Like Receptor 2AnimalsBacterial ProteinsHumansMiceMice, Inbred C57BLMyeloid Differentiation Factor 88Streptococcal InfectionsType IV Secretion SystemsBacterial ProteinsCytokinesInterferon Type IMyeloid Differentiation Factor 88Tlr2 protein, mouseToll-Like Receptor 2Type IV Secretion SystemsStreptococcus suis 2subtilisin-like protease-1Toll-like receptor 2type I interferon signaling

Identifiers

PMID39052722
PMCPMC11272045

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.