An ADAM-10 dependent EPCR shedding links meningococcal interaction with endothelial cells to purpura fulminans.

ABSTRACT: Purpura fulminans is a deadly complication of Neisseria meningitidis infections due to extensive thrombosis of microvessels. Although a Disseminated Intra-vascular Coagulation syndrome (DIC) is frequently observed during Gram negative sepsis, it is rarely associated with extensive thrombosis like those observed during meningococcemia, suggesting that the meningococcus induces a specific dysregulation of coagulation. Another specific feature of N. meningitidis pathogenesis is its ability to colonize microvessels endothelial cells via type IV pili. Importantly, endothelial cells are key in controlling the coagulation cascade through the activation of the potent anticoagulant Protein C (PC) thanks to two endothelial cell receptors among which the Endothelial Protein C Receptor (EPCR). Conside

SUBMITTER: Lecuyer H 

PROVIDER: S-EPMC5908201 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature