ArticleMedical microbiology and immunology2012
Synergistic effects of streptolysin S and streptococcal pyrogenic exotoxin B on the mouse model of group A streptococcal infection.
Article in Medical microbiology and immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Proinflammatory synergy between protease and superantigen streptococcal pyogenic exotoxins.Infection and immunity · 2025Article
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- IL-33/ST2 Axis Plays a Protective Effect inInternational journal of molecular sciences · 2021Article
- Streptococcus pyogenes infects human endometrium by limiting the innate immune response.The Journal of clinical investigation · 2021Article
- Streptolysin S induces mitochondrial damage and macrophage death through inhibiting degradation of glycogen synthase kinase-3β in Streptococcus pyogenes infection.Scientific reports · 2019Article
- HECT E3 Ubiquitin Ligase-Regulated Txnip Degradation Facilitates TLR2-Mediated Inflammation During Group A Streptococcal Infection.Frontiers in immunology · 2019Article
- β-HemolyticJournal of oral microbiology · 2019Article
- Dextromethorphan Attenuates NADPH Oxidase-Regulated Glycogen Synthase Kinase 3β and NF-κB Activation and Reduces Nitric Oxide Production in Group A Streptococcal Infection.Antimicrobial agents and chemotherapy · 2018Article
- Article
- The Transcriptional Regulator CpsY Is Important for Innate Immune Evasion in Streptococcus pyogenes.Infection and immunity · 2017Article
- Immunization with a streptococcal multiple-epitope recombinant protein protects mice against invasive group A streptococcal infection.PloS one · 2017Article
- Streptococcal pyrogenic exotoxin B inhibits apoptotic cell clearance by macrophages through protein S cleavage.Scientific reports · 2016Article
- Article
- Development of a markerless deletion system for the fish-pathogenic bacterium Flavobacterium psychrophilum.PloS one · 2015Article
- Article
- The wide world of ribosomally encoded bacterial peptides.PLoS pathogens · 2014Article
- Kallistatin modulates immune cells and confers anti-inflammatory response to protect mice from group A streptococcal infection.Antimicrobial agents and chemotherapy · 2013Article
- Determining antibody-binding site of streptococcal pyrogenic exotoxin B to protect mice from group a streptococcus infection.PloS one · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus pyogenes is a group A streptococcus (GAS) and an important human pathogen that causes a variety of diseases. Streptococcal pyrogenic exotoxin B (SPE B) and streptolysin S (SLS) are important virulence factors involved in GAS infection, but it is not clear which one is more virulent. Using an air pouch infection model, the wild-type strain NZ131, its isogenic mutants, and complementary mutants were used to examine the effects of SPE B and SLS on GAS infection. The results of the skin lesion and mouse mortality assays showed that although SPE B and SLS had a synergistic effect on GAS infection, SPE B played a more important role in local tissue damage while SLS had a more prominent effect on mouse mortality. Surveys of the exudates from the air pouch revealed that the expression of inflammatory cytokines was significantly inhibited in the sagB/speB-double-mutant JM4-infected mice. Furthermore, in vivo and in vitro studies showed that the isogenic mutant strains were more susceptible to the immune cell killing than the wild-type strain and that the sagB/speB-double-mutant JM4 was the most sensitive among these strains. Moreover, infection with the sagB/speB-double-mutant JM4 strain caused the least amount of macrophage apoptosis compared to infection with the wild-type NZ131 and the other complementary strains, which express only SPE B or SLS or both. Taken together, these results indicate that both SPE B and SLS contributed to GAS evasion from immune cell killing, local tissue damage, and mouse mortality.
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