CC17 group B Streptococcus exploits integrins for neonatal meningitis development

Group B Streptococcus (GBS) is the major cause of human neonatal infections. A single clone, designated CC17-GBS, accounts for more than 80% meningitis cases, most severe form infection. However, events allowing blood-borne GBS to penetrate brain remain largely elusive. In this study, we identified host transmembrane receptors ?5?1 and ?v?3 integrins as ligands Srr2, a CC17-GBS–specific adhesin. Two motifs located in binding region Srr2 were responsible interaction between CC17-GBS these integrins. We demonstrated blood-brain-barrier cellular model that both contributed adhesion internalization CC17-GBS. Strikingly, overexpressed during postnatal period vessels blood-brain barrier blood-cerebrospinal fluid juvenile susceptibility CC17 meningitis. Finally, blocking decreased ability cross into CNS mice an vivo Our study exploits order vessels, leading Importantly, it provides molecular insights neonate’s meningitis, thereby opening new perspectives therapeutic prevention strategies GBS-elicited