{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T02:24:47Z","timestamp":1789352687808,"version":"build-2803163510"},"reference-count":42,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,2,14]],"date-time":"2017-02-14T00:00:00Z","timestamp":1487030400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Group B <jats:italic>Streptococcus<\/jats:italic> (<jats:styled-content style=\"fixed-case\">GBS<\/jats:styled-content>) causes life\u2010threatening 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 <jats:styled-content style=\"fixed-case\">GBS<\/jats:styled-content> 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 <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>62P and activation of <jats:styled-content style=\"fixed-case\">GPII<\/jats:styled-content>b\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>a. Furthermore, the <jats:styled-content style=\"fixed-case\">GBS<\/jats:styled-content> strains that induced platelet activation also caused an increase in the expression of Toll\u2010like receptor (<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>) 2 in platelets. Pre\u2010incubation of platelets with anti\u2010<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2 monoclonal antibody, but not anti\u2010<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 monoclonal antibody, inhibited these functional responses induced by <jats:styled-content style=\"fixed-case\">GBS<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2 stimulation also activated the phosphoinositide 3\u2010kinase (<jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3\u2010K)\/Akt signalling pathway in platelets, and inhibition of <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3\u2010K significantly reduced <jats:styled-content style=\"fixed-case\">GBS<\/jats:styled-content>\u2010induced platelet responses. Our results indicate that three of the <jats:styled-content style=\"fixed-case\">GBS<\/jats:styled-content> strains from the septic patients can trigger platelet activation by interacting with platelets, which involves the elevation of platelet <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2 expression.<\/jats:p>","DOI":"10.1111\/1440-1681.12707","type":"journal-article","created":{"date-parts":[[2016,11,25]],"date-time":"2016-11-25T07:02:52Z","timestamp":1480057372000},"page":"335-343","source":"Crossref","is-referenced-by-count":20,"title":["Strains of Group B streptococci from septic patients induce platelet activation via Toll\u2010like Receptor 2"],"prefix":"10.1111","volume":"44","author":[{"given":"Xiaoyan","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Hematology Sun Yat\u2010sen Memorial Hospital Sun Yat\u2010sen University  Guangzhou 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