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Streptococcus sanguinis‐induced cytokine release from platelets
Author(s) -
MCNICOL A.,
AGPALZA A.,
JACKSON E. C. G.,
HAMZEHCOGNASSE H.,
GARRAUD O.,
COGNASSE F.
Publication year - 2011
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2011.04462.x
Subject(s) - streptococcus sanguinis , platelet , platelet activation , cytokine , immune system , platelet factor 4 , epinephrine , microbiology and biotechnology , chemistry , immunology , biology , biofilm , bacteria , endocrinology , genetics
Summary. Background: There is increasing evidence that both chronic and acute infections play a role in the development and progression of atherothrombotic disorders. One potential mechanism is the direct activation of platelets by bacteria. A wide range of bacterial species activate platelets through heterogeneous mechanisms. The oral micro‐organism S. sanguinis stimulates platelet aggregation in vitro in a strain‐dependent manner, although there are no reports of associated cytokine production. Objective: The aim of the present study was to determine whether platelet activation by S. sanguinis involved the release of pro‐inflammatory and immune modulating factors, and whether activation was enhanced by epinephrine. Methods and results: Four strains of S. sanguinis and one of S. gordonii stimulated the release of RANTES, PF4, sCD40L and PDGF‐AB, whereas only one S. sanguinis strain caused the release of sCD62p. Epinephrine enhanced S. sanguinis ‐induced platelet aggregation and phosphorylation of phospholipase Cγ2 and Erk, but inhibited RANTES, PF4, sCD40L and PDGF‐AB release. Wortmannin inhibited S. sanguinis ‐induced aggregation and release; however, only aggregation was partially reversed by epinephrine. Conclusions: The present study demonstrates that platelets respond to S. sanguinis with both prothrombotic and pro‐inflammatory/immune‐modulating responses. Epinephrine, potentially released in response to infection and/or stress, can significantly enhance the prothrombotic response, thereby providing a putative link between bacteraemia and acute coronary events during stress. In contrast, epinephrine inhibited the pro‐inflammatory/immune‐modulating response by an undetermined mechanism.