ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
Acquisition of factor H by a novel surface protein on group B Streptococcus promotes complement degradation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- An opportunistic pathogen under stress: how Group B Streptococcus responds to cytotoxic reactive species and conditions of metal ion imbalance to survive.FEMS microbiology reviews · 2024Review
- Group BJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Inactivation of theVirulence · 2020Article
- Glycine, serine and threonine metabolism confounds efficacy of complement-mediated killing.Nature communications · 2019Article
- Defining the Role of theJournal of bacteriology · 2019Article
- The Streptococcus agalactiae complement interfering protein combines multiple complement-inhibitory mechanisms by interacting with both C4 and C3 ligands.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches.Frontiers in pediatrics · 2018Review
- The Adc/Lmb System Mediates Zinc Acquisition in Streptococcus agalactiae and Contributes to Bacterial Growth and Survival.Journal of bacteriology · 2016Article
- Utilizing complement evasion strategies to design complement-based antibacterial immunotherapeutics: Lessons from the pathogenic Neisseriae.Immunobiology · 2016Review
- The Group B Streptococcus-Secreted Protein CIP Interacts with C4, Preventing C3b Deposition via the Lectin and Classical Complement Pathways.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Single nucleotide resolution RNA-seq uncovers new regulatory mechanisms in the opportunistic pathogen Streptococcus agalactiae.BMC genomics · 2015Article
- Molecular basis of host specificity in human pathogenic bacteria.Emerging microbes & infections · 2014Review
- Metal binding is critical for the folding and function of laminin binding protein, Lmb of Streptococcus agalactiae.PloS one · 2013Article
- Insight into the evolution of the histidine triad protein (HTP) family in Streptococcus.PloS one · 2013Article
- Preclinical evaluation of the Pht proteins as potential cross-protective pneumococcal vaccine antigens.Infection and immunity · 2011Article
- Fcγ receptor I alpha chain (CD64) expression in macrophages is critical for the onset of meningitis by Escherichia coli K1.PLoS pathogens · 2010Article
- The Streptococcus pneumoniae capsule inhibits complement activity and neutrophil phagocytosis by multiple mechanisms.Infection and immunity · 2010Article
- Parallel Evolution of Group BmSystemsArticle
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Binding of the host complement regulator, factor H (FH), by some pathogenic microbes constitutes an important virulence mechanism, whereby complement is broken down to help microbes survive in the host. Although it has been hypothesized for the past two decades that GBS type III binds FH via sialic acid present on its capsule, neither the binding of FH to GBS has been demonstrated nor the mechanism of interaction identified. We observed that FH bound to both wild-type and capsule or sialic acid-deficient GBS that were used as negative controls. Wild-type and acapsular GBS were incubated with serum or pure FH degraded almost 90% of C3b, suggesting that the GBS-bound FH maintained cofactor activity. In addition, dot-blot analysis showed approximately 5-10% of C5 and C9 formation, as compared to an Escherichia coli control, suggesting breakdown at the C3b level. Protease treatment of the bacteria completely abolished binding of FH. Using overlay assays and mass spectroscopic analysis, we identified the FH receptor as the streptococcal histidine triad (SHT) surface protein. The ability of binding FH to SHT was further confirmed by using recombinant SHT. This report describes the identification of the SHT as an FH-binding protein on the surface of GBS type III, revealing a novel mechanism by which the bacterium acquires FH to evade complement opsonization.
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Registered trials
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.