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Strains of Group B streptococci from septic patients induce platelet activation via Toll‐like Receptor 2
Author(s) -
Liu Xiaoyan,
Liu Hongyun,
Luo Xianming,
Zhang Ping,
Gao Yanmin,
Xie Shuangfeng,
Xu Kang,
Chang Jianxing,
Ma Liping
Publication year - 2017
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12707
Subject(s) - platelet , platelet activation , tlr2 , sepsis , receptor , monoclonal antibody , immunology , chemistry , tlr4 , microbiology and biotechnology , medicine , biology , antibody
Summary Group B Streptococcus ( GBS ) causes life‐threatening bacterial sepsis, especially in newborns and pregnant women. Patients suffering from sepsis often display low platelet counts, characterized by thrombocytopenia, because of platelet activation. In the present study, the roles of six GBS strains from septic patients in platelet aggregation, as well as the underlying mechanisms, were investigated. Incubation of platelets with three of the strains induced platelet aggregation, increased the secretion of cellular adhesin molecule CD 62P and activation of GPII b/ III a. Furthermore, the GBS strains that induced platelet activation also caused an increase in the expression of Toll‐like receptor ( TLR ) 2 in platelets. Pre‐incubation of platelets with anti‐ TLR 2 monoclonal antibody, but not anti‐ TLR 4 monoclonal antibody, inhibited these functional responses induced by GBS . TLR 2 stimulation also activated the phosphoinositide 3‐kinase ( PI 3‐K)/Akt signalling pathway in platelets, and inhibition of PI 3‐K significantly reduced GBS ‐induced platelet responses. Our results indicate that three of the GBS strains from the septic patients can trigger platelet activation by interacting with platelets, which involves the elevation of platelet TLR 2 expression.