ArticleInfection and immunity2005
Adherence to and invasion of human brain microvascular endothelial cells are promoted by fibrinogen-binding protein FbsA of Streptococcus agalactiae.
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 43 papers.
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Who cites it
43 citing papers in PubMed.
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- Mechanisms and Manifestations of Group B Streptococcus Meningitis in Newborns.Journal of the Pediatric Infectious Diseases Society · 2025Review
- Re-framing the importance of Group BInfection and immunity · 2024Review
- An unusual imaging presentation of pediatric bacterial meningoencephalitis: a case-report study.Annals of medicine and surgery (2012) · 2024Article
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- Group B Streptococcal Neonatal Meningitis.Clinical microbiology reviews · 2022Review
- Molecular epidemiology, drug resistance, and virulence gene analysis ofFrontiers in cellular and infection microbiology · 2022Article
- Virulence factors ofFrontiers in microbiology · 2022Review
- Potential factors involved in the early pathogenesis of Streptococcus uberis mastitis: a review.Folia microbiologica · 2021Review
- Bacterial protein domains with a novel Ig-like fold target human CEACAM receptors.The EMBO journal · 2021Article
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- Association between genotypic diversity and biofilm production in group B Streptococcus.BMC microbiology · 2016Article
- Catecholamine-Stimulated Growth ofFrontiers in cellular and infection microbiology · 2016Article
- Streptococcus agalactiae infection in zebrafish larvae.Microbial pathogenesis · 2015Article
- Interaction of fibrinogen and muramidase-released protein promotes the development of Streptococcus suis meningitis.Frontiers in microbiology · 2015Article
- The role of autophagy during group B Streptococcus infection of blood-brain barrier endothelium.The Journal of biological chemistry · 2014Article
- Pathogens penetrating the central nervous system: infection pathways and the cellular and molecular mechanisms of invasion.Clinical microbiology reviews · 2014Review
- FbsC, a novel fibrinogen-binding protein, promotes Streptococcus agalactiae-host cell interactions.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
5 authors.
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Abstract
Streptococcus agalactiae is a frequent cause of bacterial sepsis and meningitis in neonates. During the course of infection, S. agalactiae colonizes and invades a number of host compartments, thereby interacting with different host tissues. Deletion of the fbsA gene, encoding the fibrinogen protein FbsA, significantly impaired the adherence and invasion of human brain microvascular endothelial cells (HBMEC) by S. agalactiae. The adherence and invasiveness of an fbsA deletion mutant were restored by reintroducing the fbsA gene on an expression vector. Heterologous expression of fbsA in Lactococcus lactis enabled this bacterium to adhere to but not to invade HBMEC, suggesting that FbsA is a streptococcal adhesin. Finally, host cell adherence and invasion were significantly blocked in competition experiments with either purified FbsA fusion protein or a monoclonal antibody directed against the fibrinogen-binding epitope of FbsA. The S. agalactiae fbsA mutant induced a release of the neutrophil chemoattractant interleukin-8 (IL-8) equal to that induced by the wild type. Taken together, our studies demonstrate that FbsA promotes the adherence of S. agalactiae to HBMEC but that FbsA neither mediates the bacterial invasion into host cells nor plays a role in IL-8 release for HBMEC.
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