ArticleMolecular microbiology2014
The relationship of the lipoprotein SsaB, manganese and superoxide dismutase in Streptococcus sanguinis virulence for endocarditis.
Article in Molecular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 60 citations in OpenAlex.
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- A widespread family of molecular chaperones promotes the intracellular stability of type VIIb secretion system-exported toxins.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Biochemical and structural characterization of a reactive intermediate deaminase A homolog from Streptococcus sanguinis.Scientific reports · 2025Article
- Manganese uptake by MtsABC contributes to the pathogenesis of human pathogen group A streptococcus by resisting host nutritional immune defenses.Infection and immunity · 2024Article
- A novel infective endocarditis virulence factor related to multiple functions for bacterial survival in blood was discovered inbioRxiv : the preprint server for biology · 2024Article
- Determinants of bacterial survival and proliferation in blood.FEMS microbiology reviews · 2024Review
- Ethanol extract from Astilbe chinensis inflorescence suppresses inflammation in macrophages and growth of oral pathogenic bacteria.PloS one · 2024Article
- Environmental influences on Streptococcus sanguinis membrane vesicle biogenesis.The ISME journal · 2023Article
- Metal Homeostasis in Pathogenic Streptococci.Microorganisms · 2022Review
- Contribution of a ZIP-family protein to manganese uptake and infective endocarditis virulence in Streptococcus sanguinis.Molecular microbiology · 2022Article
- Manganese transport by Streptococcus sanguinis in acidic conditions and its impact on growth in vitro and in vivo.Molecular microbiology · 2022Article
- Managing Manganese: The Role of Manganese Homeostasis in Streptococcal Pathogenesis.Frontiers in cell and developmental biology · 2022Review
- Type IV Pili of Streptococcus sanguinis Contribute to Pathogenesis in Experimental Infective Endocarditis.Microbiology spectrum · 2021Article
- Proteoglycan 4 (lubricin) is a highly sialylated glycoprotein associated with cardiac valve damage in animal models of infective endocarditis.Glycobiology · 2021Article
- Time-course analysis of Streptococcus sanguinis after manganese depletion reveals changes in glycolytic and nucleic acid metabolites.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- Genome-wide identification of Streptococcus sanguinis fitness genes in human serum and discovery of potential selective drug targets.Molecular microbiology · 2021Article
- Characterization of the roles of activated charcoal and Chelex in the induction of PrfA regulon expression in complex medium.PloS one · 2021Article
- A novel sialic acid-binding adhesin present in multiple species contributes to the pathogenesis of Infective endocarditis.PLoS pathogens · 2021Article
- Intracellular Metal Speciation inACS infectious diseases · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Streptococcus sanguinis colonizes teeth and is an important cause of infective endocarditis. Our prior work showed that the lipoprotein SsaB is critical for S. sanguinis virulence for endocarditis and belongs to the LraI family of conserved metal transporters. In this study, we demonstrated that an ssaB mutant accumulates less manganese and iron than its parent. A mutant lacking the manganese-dependent superoxide dismutase, SodA, was significantly less virulent than wild-type in a rabbit model of endocarditis, but significantly more virulent than the ssaB mutant. Neither the ssaB nor the sodA mutation affected sensitivity to phagocytic killing or efficiency of heart valve colonization. Animal virulence results for all strains could be reproduced by growing bacteria in serum under physiological levels of O(2). SodA activity was reduced, but not eliminated in the ssaB mutant in serum and in rabbits. Growth of the ssaB mutant in serum was restored upon addition of Mn(2+) or removal of O(2). Antioxidant supplementation experiments suggested that superoxide and hydroxyl radicals were together responsible for the ssaB mutant's growth defect. We conclude that manganese accumulation mediated by the SsaB transport system imparts virulence by enabling cell growth in oxygen through SodA-dependent and independent mechanisms.
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