ArticleInfection and immunity2003
Subtractive hybridization identifies a novel predicted protein mediating epithelial cell invasion by virulent serotype III group B Streptococcus agalactiae.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 54 citations in OpenAlex.
- Role of pilus proteins in adherence and invasion of Streptococcus agalactiae to the lung and cervical epithelial cells.The Journal of biological chemistry · 2013Trial
- The serine protease HtrA regulates Group B Streptococcus virulence and affects the host response to infection.PLoS pathogens · 2025Article
- Infection of endothelial cells by Streptococcus agalactiae reveals potential role of PI-2b pilus on endothelial barrier dysfunction.Memorias do Instituto Oswaldo Cruz · 2025Article
- Specific interaction between Group BInfection and immunity · 2024Article
- Phenotypic changes in group B streptococci grown in the presence of the polyols, erythritol, sorbitol and mannitol.BMC microbiology · 2021Article
- Multidrug Resistance and Molecular Characterization ofFrontiers in cellular and infection microbiology · 2021Article
- Complete Genome Sequence of Serotype IIIGenome announcements · 2017Article
- Contribution of pilus type 2b to invasive disease caused by a Streptococcus agalactiae ST-17 strain.BMC microbiology · 2017Article
- Streptococcus agalactiae from pregnant women: antibiotic and heavy-metal resistance mechanisms and molecular typing.Epidemiology and infection · 2016Article
- Article
- Association and virulence gene expression vary among serotype III group B streptococcus isolates following exposure to decidual and lung epithelial cells.Infection and immunity · 2014Article
- Associations between capsular serotype, multilocus sequence type, and macrolide resistance in Streptococcus agalactiae isolates from Japanese infants with invasive infections.Epidemiology and infection · 2014Article
- The two-component response regulator LiaR regulates cell wall stress responses, pili expression and virulence in group B Streptococcus.Microbiology (Reading, England) · 2013Article
- Phylogenetic lineage and pilus protein Spb1/SAN1518 affect opsonin-independent phagocytosis and intracellular survival of Group B Streptococcus.Microbes and infection · 2011Article
- Streptococcus adherence and colonization.Microbiology and molecular biology reviews : MMBR · 2009Review
- Recent advances in understanding the molecular basis of group B Streptococcus virulence.Expert reviews in molecular medicine · 2008Review
- Combining microarray technology and molecular epidemiology to identify genes associated with invasive group B streptococcus.Interdisciplinary perspectives on infectious diseases · 2008Article
- Distribution of novel and previously investigated virulence genes in colonizing and invasive isolates of Streptococcus agalactiae.Epidemiology and infection · 2007Article
- Genome analysis of multiple pathogenic isolates of Streptococcus agalactiae: implications for the microbial "pan-genome".Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Anchors away: contribution of a glycolipid anchor to bacterial invasion of host cells.The Journal of clinical investigation · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Group B Streptococcus agalactiae bacteria (group B streptococci [GBS]) are the most common cause of serious bacterial infection in newborn infants. The majority of serotype III-related cases of neonatal disease are caused by a genetically related subgroup of bacteria, restriction fragment digest pattern (RDP) type III-3, suggesting that these strains possess unique genes contributing to virulence. We used genomic subtractive hybridization to identify regions of genomic DNA unique to virulent RDP type III-3 GBS strains. Within one of these III-3-specific regions is a 1,506-bp open reading frame, spb1 (surface protein of group B streptococcus 1). A mutant type III GBS strain lacking Spb1 was constructed in virulent RDP type III-3 strain 874391, and the interactions of the wild-type and spb1 isogenic mutant with a variety of epithelial cells important to GBS colonization and infection were compared. While adherence of the spb1 isogenic mutant to A549 respiratory, C2Bbe1 colonic, and HeLa cervical epithelial cells was slightly lower than that of the 874391 strain, invasion of the Spb1(-) mutant was significantly reduced with these cell lines compared to what was seen with 874391. The defect in epithelial invasion was corrected by supplying spb1 in trans. These observations suggest that Spb1 contributes to the pathogenesis of neonatal GBS infection by mediating internalization of virulent serotype III GBS and confirm that understanding of the population structure of bacteria may lead to insights into the pathogenesis of human infections.
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