ArticlePloS one2016
Identification of CiaR Regulated Genes That Promote Group B Streptococcal Virulence and Interaction with Brain Endothelial Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- Pathogenic bacteria exploit transferrin receptor transcytosis to penetrate the blood-brain barrier.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Group B Streptococcal Neonatal Meningitis.Clinical microbiology reviews · 2022Review
- Identification of a novel cationic glycolipid in Streptococcus agalactiae that contributes to brain entry and meningitis.PLoS biology · 2022Article
- The Role and Regulatory Network of the CiaRH Two-Component System in Streptococcal Species.Frontiers in microbiology · 2021Review
- An Inventory of CiaR-Dependent Small Regulatory RNAs inFrontiers in microbiology · 2021Review
- Article
- The S Protein of Group BFrontiers in microbiology · 2021Article
- Two-Component Signal Transduction Systems in the Human Pathogen Streptococcus agalactiae.Infection and immunity · 2020Review
- The Double Life of Group B Streptococcus: Asymptomatic Colonizer and Potent Pathogen.Journal of molecular biology · 2019Review
- Cas9 Contributes to Group B Streptococcal Colonization and Disease.Frontiers in microbiology · 2019Article
- Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches.Frontiers in pediatrics · 2018Review
- Article
- Modeling Group BmSphereArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Group B Streptococcus (GBS) is a major causative agent of neonatal meningitis due to its ability to efficiently cross the blood-brain barrier (BBB) and enter the central nervous system (CNS). It has been demonstrated that GBS can invade human brain microvascular endothelial cells (hBMEC), a primary component of the BBB; however, the mechanism of intracellular survival and trafficking is unclear. We previously identified a two component regulatory system, CiaR/H, which promotes GBS intracellular survival in hBMEC. Here we show that a GBS strain deficient in the response regulator, CiaR, localized more frequently with Rab5, Rab7 and LAMP1 positive vesicles. Further, lysosomes isolated from hBMEC contained fewer viable bacteria following initial infection with the ΔciaR mutant compared to the WT strain. To characterize the contribution of CiaR-regulated genes, we constructed isogenic mutant strains lacking the two most down-regulated genes in the CiaR-deficient mutant, SAN_2180 and SAN_0039. These genes contributed to bacterial uptake and intracellular survival. Furthermore, competition experiments in mice showed that WT GBS had a significant survival advantage over the Δ2180 and Δ0039 mutants in the bloodstream and brain.
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