ArticleThe Journal of clinical investigation2021
CC17 group B Streptococcus exploits integrins for neonatal meningitis development.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Acquisition of a novel restriction modification system regulates genetic flux and gene expression in the hypervirulent and globally disseminated CC17 lineage of group B Streptococcus.Nucleic acids research · 2026Article
- Invasive Streptococcus agalactiae infections in infants in Guangzhou, Southern China (2013-2022): molecular epidemiology and clinical management implications.BMC microbiology · 2026Article
- Current knowledge and future perspectives on management and prevention of group B streptococcus in neonates and young infants.Archives of disease in childhood. Fetal and neonatal edition · 2026Review
- CRISPR1-mediated virulence and erythromycin resistance stabilization drives regional dominance ofFrontiers in cellular and infection microbiology · 2026Article
- Whole-genome characterization of neonatal group B Streptococcus infection isolates and contemporaneous maternal colonizing isolates in Southwest China.Frontiers in microbiology · 2026Article
- Group B Streptococci lyse endothelial cells to infect the brain in a zebrafish meningitis model.PLoS biology · 2025Article
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- Mechanisms and Manifestations of Group B Streptococcus Meningitis in Newborns.Journal of the Pediatric Infectious Diseases Society · 2025Review
- Neurodevelopmental impairment associated with neonatal invasive group BBrain, behavior, & immunity - health · 2024Article
- The hypervirulent Group B Streptococcus HvgA adhesin promotes central nervous system invasion through transcellular crossing of the choroid plexus.Fluids and barriers of the CNS · 2024Article
- The serine-rich repeat glycoprotein Srr2 mediates Streptococcus agalactiae interaction with host fibronectin.BMC microbiology · 2024Article
- Specific interaction between Group BInfection and immunity · 2024Article
- Engagement of αFrontiers in microbiology · 2024Article
- Crosstalk between integrin/FAK and Crk/Vps25 governs invasion of bovine mammary epithelial cells byiScience · 2023Article
- The Clinical and Genetic Characteristics ofInternational journal of molecular sciences · 2023Article
- Immunization with Multiple Virulence Factors Provides Maternal and Neonatal Protection against Group B Streptococcus Serotypes.Vaccines · 2023Article
- Conjugative transfer of streptococcal prophages harboring antibiotic resistance and virulence genes.The ISME journal · 2023Article
- Group B Streptococcus CRISPR1 Typing of Maternal, Fetal, and Neonatal Infectious Disease Isolates Highlights the Importance of CC1 inMicrobiology spectrum · 2023Article
- Molecular characteristics and antibiotic resistance mechanisms of clindamycin-resistantFrontiers in microbiology · 2023Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group B Streptococcus (GBS) is the major cause of human neonatal infections. A single clone, designated CC17-GBS, accounts for more than 80% of meningitis cases, the most severe form of the infection. However, the events allowing blood-borne GBS to penetrate the brain remain largely elusive. In this study, we identified the host transmembrane receptors α5β1 and αvβ3 integrins as the ligands of Srr2, a major CC17-GBS-specific adhesin. Two motifs located in the binding region of Srr2 were responsible for the interaction between CC17-GBS and these integrins. We demonstrated in a blood-brain-barrier cellular model that both integrins contributed to the adhesion and internalization of CC17-GBS. Strikingly, both integrins were overexpressed during the postnatal period in the brain vessels of the blood-brain barrier and blood-cerebrospinal fluid barrier and contributed to juvenile susceptibility to CC17 meningitis. Finally, blocking these integrins decreased the ability of CC17-GBS to cross into the CNS of juvenile mice in an in vivo model of meningitis. Our study demonstrated that CC17-GBS exploits integrins in order to cross the brain vessels, leading to meningitis. Importantly, it provides host molecular insights into neonate's susceptibility to CC17-GBS meningitis, thereby opening new perspectives for therapeutic and prevention strategies of GBS-elicited meningitis.
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