ArticleFrontiers in microbiology2015
Toll-like receptor 4 confers inflammatory response to Suilysin.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Innate immune response to Streptococcus suis infection: advances and future challenges.Veterinary research · 2026Review
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
- Current prevalence and therapeutic strategies for porcineApplied and environmental microbiology · 2025Review
- Dihydroartemisinin ameliorates innate inflammatory response induced byJournal of pharmaceutical analysis · 2023Article
- Cholesterol dependent cytolysins and the brain: Revealing a potential therapeutic avenue for bacterial meningitis.AIMS microbiology · 2023Review
- Suilyin Disrupts the Blood-Brain Barrier by Activating Group III Secretory Phospholipase A2.Life (Basel, Switzerland) · 2022Article
- Acquiring high expression of suilysin enable non-epidemicEmerging microbes & infections · 2021Article
- ATP Facilitates Staphylococcal Enterotoxin O Induced Neutrophil IL-1β SecretionFrontiers in immunology · 2021Article
- TRIM32 Drives Pathogenesis in Streptococcal Toxic Shock-Like Syndrome and Streptococcus suis Meningitis by Regulating Innate Immune Responses.Infection and immunity · 2020Article
- Inhibitory Effect of Piceatannol onFrontiers in microbiology · 2020Article
- The Impact of SsPI-1 Deletion onPathogens (Basel, Switzerland) · 2019Article
- Interleukin-1 signaling induced by Streptococcus suis serotype 2 is strain-dependent and contributes to bacterial clearance and inflammation during systemic disease in a mouse model of infection.Veterinary research · 2019Article
- An NLRP3 inflammasome-triggered cytokine storm contributes to Streptococcal toxic shock-like syndrome (STSLS).PLoS pathogens · 2019Article
- Listeriolysin O: A phagosome-specific cytolysin revisited.Cellular microbiology · 2019Review
- Article
- Antigen I/II Participates in the Interactions ofFrontiers in cellular and infection microbiology · 2019Article
- Triggering Receptor Expressed on Myeloid Cells-1 Signaling: Protective and Pathogenic Roles on Streptococcal Toxic-Shock-Like Syndrome Caused byFrontiers in immunology · 2018Review
- Interaction of factor H-binding protein of Streptococcus suis with globotriaosylceramide promotes the development of meningitis.Virulence · 2017Article
- Type I Interferon Induced byFrontiers in immunology · 2017Article
- Effects of Suilysin onFrontiers in cellular and infection microbiology · 2016Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus suis serotype 2 (SS2) is an emerging human pathogen worldwide. A large outbreak occurred in the summer of 2005 in China. Serum samples from this outbreak revealed that levels of the main proinflammatory cytokines were significantly higher in patients with streptococcal toxic-shock-like syndrome (STSLS) than in patients with meningitis only. However, the mechanism underlying the cytokine storm in STSLS caused by SS2 remained unclear. In this study, we found that suilysin (SLY) is the main protein inflammatory stimulus of SS2 and that native SLY (nSLY) stimulated cytokines independently of its haemolytic ability. Interestingly, a small amount of SLY (Å Mol/L) induced strong, long-term TNF-α release from human PBMCs. We also found that nSLY stimulated TNF-α in wild-type macrophages but not in macrophages from mice that carried a spontaneous mutation in TLR4 (P712H). We demonstrated for the first time that SLY stimulates immune cells through TLR4. In addition, the Myd88 adaptor-p38-MAPK pathway was involved in this process. The present study suggested that the TLR4-dependent inflammatory responses induced by SLY in host might contribute to the STSLS caused by SS2 and that p38-MAPK could be used as a target to control the release of excess TNF-α induced by SS2.
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Registered trials
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.