ArticlePLoS pathogens2019
An NLRP3 inflammasome-triggered cytokine storm contributes to Streptococcal toxic shock-like syndrome (STSLS).
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses that pooled it.
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Who cites it
76 citing papers in PubMed, 2 syntheses or guidelines pooled it, 128 citations in OpenAlex.
- Two Birds with One Stone: Drug Regime Targets Viral Pathogenesis Phases and COVID-19 ARDS at the Same Time.Infectious disorders drug targets · 2024Pooled it
- Identification ofVirulence · 2021Pooled it
- The IL-17A/Neutrophil axis plays a critical role in lethal infection induced by an emerging ultra-virulentVirulence · 2026Article
- Innate immune response to Streptococcus suis infection: advances and future challenges.Veterinary research · 2026Review
- The cholesterol-dependent cytolysin promotesInfection and immunity · 2026Article
- Article
- Cathelicidin CATH-2 suppresses the NF-κB/ROS/NLRP3 signaling pathway via regulating mTOR-dependent autophagy during Streptococcus suis infection.Veterinary research · 2026Article
- [Research progress on toxic shock syndrome due to group AZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- The NLRP3 inflammasome as a key pathway in the affective and chronic fatigue symptoms of Long COVID.Journal of translational medicine · 2026Article
- Article
- EP300 confers protection against acute pancreatitis via acetylating HSF1 and promoting PRKN-mediated mitophagy in pancreatic acinar cells.Cell communication and signaling : CCS · 2025Article
- RfeA from Streptococcus suis serotype 2 triggers NLRP3/Caspase-1-dependent pyroptosis leading to blood-brain barrier disruption.Veterinary research · 2025Article
- Review
- The conserved transcription factor PrlP modulates colonization and pathogenicity of Streptococcus suis in response to environmental stress.PLoS pathogens · 2025Article
- Antibiotics re-booted-time to kick back against drug resistance.npj antimicrobials and resistance · 2025Review
- Population Genomics, Virulence Traits, and Antimicrobial Resistance ofMicroorganisms · 2025Article
- Jinxin oral liquid reduced lung inflammation in influenza A virus infected mice through inhibiting NOD-like receptor protein 3 pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Identification of SepF in Streptococcus suis involving cell division.BMC microbiology · 2025Article
- Current prevalence and therapeutic strategies for porcineApplied and environmental microbiology · 2025Review
- Computational study on the mechanism of small molecules inhibiting NLRP3 with ensemble docking and molecular dynamic simulations.BMC pharmacology & toxicology · 2025Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with the Streptococcus suis (S. suis) epidemic strain can cause Streptococcal toxic shock-like syndrome (STSLS), which is characterized by a cytokine storm, dysfunction of multiple organs and a high incidence of mortality despite adequate treatment. Despite some progress concerning the contribution of the inflammatory response to STSLS, the precise mechanism underlying STSLS development remains elusive. Here, we use a murine model to demonstrate that caspase-1 activity is critical for STSLS development. Furthermore, we show that inflammasome activation by S. suis is mainly dependent on NLRP3 but not on NLRP1, AIM2 or NLRC4. The important role of NLRP3 activation in STSLS is further confirmed in vivo with the NLRP3 inhibitor MCC950 and nlrp3-knockout mice. By comparison of WT strain with isogenic strains with mutation of various virulence genes for inflammasome activation, Suilysin is essential for inflammasome activation, which is dependent on the membrane perforation activity to cause cytosolic K+ efflux. Moreover, the mutant strain msly (P353L) expressing mutagenic SLY without hemolytic activity was unable to activate the inflammasome and does not cause STSLS. In summary, we demonstrate that the high membrane perforation activity of the epidemic strain induces a high level of NLRP3 inflammasome activation, which is essential for the development of the cytokine storm and multi-organ dysfunction in STSLS and suggests NLRP3 inflammasome as an attractive target for the treatment of STSLS.
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