Complement C3b contributes to Escherichia coli-induced platelet aggregation in human whole blood.

ABSTRACT:

Introduction

Platelets have essential functions as first responders in the immune response to pathogens. Activation and aggregation of platelets in bacterial infections can lead to life-threatening conditions such as arterial thromboembolism or sepsis-associated coagulopathy.

Methods

In this study, we investigated the role of complement in Escherichia coli (E. coli)-induced platelet aggregation in human whole blood, using Multiplate^® aggregometry, flow cytometry, and confocal microscopy.

Results and discussion

We found that compstatin, which inhibits the cleavage of complement component C3 to its components C3a and C3b, reduced the E. coli-induced platelet aggregation by 42%-76% (p = 0.0417). This C3-dependent aggregation was not C3a-me

SUBMITTER: Landsem A 

PROVIDER: S-EPMC9797026 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature