Streptococcus pneumoniae From Patients With Hemolytic Uremic Syndrome Binds Human Plasminogen via the Surface Protein PspC and Uses Plasmin to Damage Human Endothelial Cells.

Abstract:

Pneumococcal hemolytic uremic syndrome (HUS) in children is caused by infections with Streptococcus pneumoniae. Because endothelial cell damage is a hallmark of HUS, we studied how HUS-inducing pneumococci derived from infant HUS patients during the acute phase disrupt the endothelial layer. HUS pneumococci efficiently bound human plasminogen. These clinical isolates of HUS pneumococci efficiently bound human plasminogen via the bacterial surface proteins Tuf and PspC. When activated to plasmin at the bacterial surface, the active protease degraded fibrinogen and cleaved C3b. Here, we show that PspC is a pneumococcal plasminogen receptor and that plasmin generated on the surface of HUS pneumococci damages endothelial cells, causing endothelial retraction and exposure of the underlying matrix. Thus, HUS pneumococci damage endothelial cells in the blood vessels and disturb local complement homeostasis. Thereby, HUS pneumococci promote a thrombogenic state that drives HUS pathology.

SEEK ID: https://funginet.hki-jena.de/publications/158

PubMed ID: 28968817

Projects: B4, FungiNet C - Candida projects

Journal: J Infect Dis

Citation: J Infect Dis. 2018 Jan 17;217(3):358-370. doi: 10.1093/infdis/jix305.

Date Published: 17th Jan 2018

Authors: C. Meinel, G. Sparta, H. M. Dahse, F. Horhold, R. Konig, M. Westermann, S. M. Coldewey, Z. Cseresnyes, Marc Thilo Figge, S. Hammerschmidt, Christine Skerka, Peter Zipfel

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Created: 16th Feb 2021 at 16:07

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