Dual actions of group B Streptococcus capsular sialic acid provide resistance to platelet-mediated antimicrobial killing.

ABSTRACT: Circulating platelets have important functions in thrombosis and in modulating immune and inflammatory responses. However, the role of platelets in innate immunity to bacterial infection is largely unexplored. While human platelets rapidly kill Staphylococcus aureus, we found the neonatal pathogen group B Streptococcus (GBS) to be remarkably resistant to platelet killing. GBS possesses a capsule polysaccharide (CPS) with terminal α2,3-linked sialic acid (Sia) residues that mimic a common epitope present on the human cell surface glycocalyx. A GBS mutant deficient in CPS Sia was more efficiently killed by human platelets, thrombin-activated platelet releasate, and synthetic platelet-associated antimicrobial peptides. GBS Sia is known to bind inhibitory Sia-recognizing Ig super

SUBMITTER: Uchiyama S 

PROVIDER: S-EPMC6462088 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature