ArticleMolecular medicine reports2014
Increased production of suilysin contributes to invasive infection of the Streptococcus suis strain 05ZYH33.
Article in Molecular medicine reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Identification ofVirulence · 2021Pooled it
- Population Genomics, Virulence Traits, and Antimicrobial Resistance ofMicroorganisms · 2025Article
- New Insights into Neutrophil Extracellular Trap (NETs) Formation from Porcine Neutrophils in Response to Bacterial Infections.International journal of molecular sciences · 2022Article
- Acquiring high expression of suilysin enable non-epidemicEmerging microbes & infections · 2021Article
- Neutrophils inMicroorganisms · 2021Review
- Phenotype and multi-omics comparison of Staphylococcus and Streptococcus uncovers pathogenic traits and predicts zoonotic potential.BMC genomics · 2021Article
- All major cholesterol-dependent cytolysins use glycans as cellular receptors.Science advances · 2020Article
- Contribution of Nlrp3 Inflammasome Activation Mediated by Suilysin to Streptococcal Toxic Shock-like Syndrome.Frontiers in microbiology · 2020Article
- Membrane Binding, Cellular Cholesterol Content and Resealing Capacity Contribute to Epithelial Cell Damage Induced by Suilysin ofPathogens (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
- Amentoflavone Ameliorates Streptococcus suis-Induced InfectionApplied and environmental microbiology · 2018Article
- The involvement of MsmK in pathogenesis of the Streptococcus suis serotype 2.MicrobiologyOpen · 2017Article
- Suilysin-induced Platelet-Neutrophil Complexes Formation is Triggered by Pore Formation-dependent Calcium Influx.Scientific reports · 2016Article
- Streptococcus suis in invasive human infections in Poland: clonality and determinants of virulence and antimicrobial resistance.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016Article
- A hypothetical model of host-pathogen interaction of Streptococcus suis in the gastro-intestinal tract.Gut microbes · 2016Review
- Effects of Suilysin onFrontiers in cellular and infection microbiology · 2016Article
- Suilysin Stimulates the Release of Heparin Binding Protein from Neutrophils and Increases Vascular Permeability in Mice.Frontiers in microbiology · 2016Article
- Toll-like receptor 4 confers inflammatory response to Suilysin.Frontiers in microbiology · 2015Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus suis serotype 2 (SS2) is widely recognized in the veterinary world as the cause of rapidly progressive and fatal sepsis in infant pigs, manifested with meningitis, polyarthritis and pneumonia. It has evolved into a highly infectious strain, and caused two large-scale outbreaks of human epidemic in China, characterized bytypical toxic-shock syndrome and invasive infection. However, the molecular basis of virulence of this emerging zoonotic pathogen is still largely unknown. The present study shows that the sequence type (ST)7 epidemic strain S. suis 05ZYH33 causes higher mortality, higher necrosis of polymorphonuclear neutrophils and a significantly higher damage to human umbilical vein endothelial cells compared to the non-epidemic strain S. suis 1940. These differences appear to associate with the enhanced secretion of suilysin (sly) by S. suis 05ZYH33 compared to the non-epidemic strain 1940. Inclusion of additional strains confirmed that the epidemic ST7 strains produce more sly protein (mean, 1.49 g/ml; range, 0.76‑1.91 g/ml) than non‑epidemic strains (mean, 0.33 g/ml; range, 0.07-0.94 g/ml), and this difference is significant (P<0.001). The nonpolar mutant strain S. suis Δsly, constructed from the epidemic ST7 strain S. suis 05ZYH33 confirmed the role of sly on the enhanced virulence of S. suis ST7 strains. These findings suggest that increased sly production in S. suis 05ZYH33 facilitates penetration to the epithelium and its survival in the bloodstream, thereby contributing to the invasive infection.
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