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Platelet α‐granules modulate the inflammatory response under systemic lipopolysaccharide injection in mice
Author(s) -
Tariket Sofiane,
Guerrero Jose A.,
Garraud Olivier,
Ghevaert Cedric,
Cognasse Fabrice
Publication year - 2019
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/trf.14970
Subject(s) - inflammation , platelet , lipopolysaccharide , proinflammatory cytokine , hemostasis , platelet activation , medicine , immunology , systemic inflammation , monocyte
BACKGROUND Beyond their role in hemostasis and thrombosis, platelets are also important mediators of inflammation by the release of hundreds of factors stored in their α‐granules. Mutations in Nbeal2 cause gray platelet syndrome (GPS), characterized by the lack of platelet α‐granules. This study aims to evaluate the immunological (proinflammatory) effects of platelet α‐granules. STUDY DESIGN AND METHODS We performed an experiment using Nbeal2 −/− mice, the mouse model of GPS. Systemic inflammation was induced by intravenous injection of lipopolysaccharide (LPS). Inflammatory response was assessed by quantification of inflammatory soluble factors and platelet biological response modifiers. RESULTS The lack of Nbeal2 (in Nbeal2 −/− mice, compared with controls) significantly reduced the recruitment of circulating neutrophils and monocytes. Moreover, after LPS injection, there was a significant increase in neutrophil and monocyte counts in control animals, compared with Nbeal2 −/− mice. The control of inflammation, evaluated by the production of anti‐inflammatory cytokines, appeared to be greater in Nbeal2 −/− mice compared with controls. Conversely, the production of certain inflammatory‐soluble mediators known to characterize normal platelet secretion, such as soluble CD40 ligand (sCD40L), was decreased under experimental inflammation in Nbeal2 −/− mice. CONCLUSIONS These results show that α‐granules play a direct role in platelet‐mediated inflammation balance, confirming the need to further investigate platelet‐associated inflammatory pathophysiology and inflammatory adverse events related to blood transfusion.