ArticleInfection and immunity2005
Glucosyltransferases of viridans streptococci are modulins of interleukin-6 induction in infective endocarditis.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- Cell wall glycosyltransferase ofInfection and immunity · 2025Article
- Oral streptococci: modulators of health and disease.Frontiers in cellular and infection microbiology · 2024Review
- Roles ofFrontiers in microbiology · 2024Review
- Article
- Potential Advances of Adjunctive Hyperbaric Oxygen Therapy in Infective Endocarditis.Frontiers in cellular and infection microbiology · 2022Review
- PspC domain-containing protein (PCP) determines Streptococcus mutans biofilm formation through bacterial extracellular DNA release and platelet adhesion in experimental endocarditis.PLoS pathogens · 2021Article
- Ursolic Acid Targets Glucosyltransferase and Inhibits Its Activity to PreventFrontiers in microbiology · 2021Article
- Strain-dependent interactions of Streptococcus gallolyticus subsp. gallolyticus with human blood cells.BMC microbiology · 2017Article
- AtlA Mediates Extracellular DNA Release, Which Contributes to Streptococcus mutans Biofilm Formation in an Experimental Rat Model of Infective Endocarditis.Infection and immunity · 2017Article
- Article
- Activated human valvular interstitial cells sustain interleukin-17 production to recruit neutrophils in infective endocarditis.Infection and immunity · 2015Article
- Contribution of the interaction of Streptococcus mutans serotype k strains with fibrinogen to the pathogenicity of infective endocarditis.Infection and immunity · 2014Article
- Genetic variants in genes of the inflammatory response in association with infective endocarditis.PloS one · 2014Article
- Comparative genome analysis of Streptococcus infantarius subsp. infantarius CJ18, an African fermented camel milk isolate with adaptations to dairy environment.BMC genomics · 2013Article
- The collagen-binding protein Cnm is required for Streptococcus mutans adherence to and intracellular invasion of human coronary artery endothelial cells.Infection and immunity · 2011Article
- Article
- Lack of the delta subunit of RNA polymerase increases virulence related traits of Streptococcus mutans.PloS one · 2011Article
- Interactions between endocarditis-derived Streptococcus gallolyticus subsp. gallolyticus isolates and human endothelial cells.BMC microbiology · 2010Article
- New concepts in the pathophysiology of infective endocarditis.Current infectious disease reports · 2006Article
- Glucosyltransferases of viridans group streptococci modulate interleukin-6 and adhesion molecule expression in endothelial cells and augment monocytic cell adherence.Infection and immunity · 2006Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glucosyltransferases (GTFs) of viridans streptococci, common pathogens of infective endocarditis, are extracellular proteins that convert sucrose into exopolysaccharides and glucans. GTFs B, C, and D of Streptococcus mutans are modulins that induce, in vitro and in vivo, the production of cytokines, in particular interleukin-6 (IL-6), from monocytes. The roles of S. mutans GTFs in infectivity and inflammation in situ were tested in a rat experimental model of endocarditis. No significant differences in infectivity, in terms of 95% infective dose and densities of bacteria inside vegetations, were observed between laboratory strain GS-5 and two clinical isolates or isogenic mutant NHS1DD, defective in the expression of GTFs. In aortic valves and surrounding tissues, IL-6 was detected by Western blots and immunostaining 24 h after GS-5 infection, was maintained over 72 h, and was followed by production of tumor necrosis factor alpha but not IL-1beta. Animals infected with NHS1DD showed markedly lower levels of IL-6 (less than 5% of that of parental GS-5-infected rats), while tumor necrosis factor alpha was unaffected. In contrast, animals infected with NHR1DD, another isogenic mutant expressing only GtfB, showed a much smaller reduction (down to 56%). These results suggest that GTFs are specific modulins that act during acute inflammation, inducing IL-6 from endothelial cells surrounding the infected valves without affecting bacterial colonization in vegetations, and that IL-6 might persist in chronic inflammation in endocarditis.
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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.