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BMC Microbiol. 2017 Jul 3;17(1):148. doi: 10.1186/s12866-017-1057-8.

Contribution of pilus type 2b to invasive disease caused by a Streptococcus agalactiae ST-17 strain.

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GSK S.r.l., Siena, Italy.
Department of Biology and Center for Microbial Sciences, San Diego State University, 5500 Campanile Dr., NLS 317, San Diego, CA, 92182, USA.
Department of Pediatrics, University of California San Diego School of Medicine, La Jolla, CA, 92093, USA.
GSK S.r.l., Siena, Italy.



Group B Streptococcus (GBS) is a major cause of invasive disease especially in neonates. In GBS three structurally distinct pilus polymers have been identified as important virulence factors and promising vaccine candidates. The vast majority of Group B Streptococci belonging to the hypervirulent serotype III ST-17 lineage bear pilus types 1 and 2b. The purpose of this study was to investigate the relative contribution of these two pilus types to the pathogenesis of a ST-17 strain.


We performed in vivo and in vitro analysis of isogenic knockout mutants derived from the GBS COH1 ST-17 strain deprived of either pilus type 1 or 2b. We compared the two pilus mutants with the wild type strain in a mouse model of invasive disease, in vitro survival in macrophages, and adherence/invasion assays using human brain endothelial and lung epithelial cell lines. Significantly less of the pilus 2b mutant was recovered from the blood, lungs and brain tissue of infected mice compared to the wild-type and pilus 1 mutant strains. Further, while the pilus 2b mutant survived similarly in murine macrophages, it exhibited a lower capacity to adhere and invade human brain epithelial and lung endothelial cell lines.


The data suggest an important role of pilus 2b in mediating GBS infection and host cell interaction of strains belonging to the hypervirulent GBS ST-17 lineage.


GBS; Host cell adherence; Host cell invasion; Mouse meningitis model; Pilus island; Pilus protein; Streptococcus agalactiae

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