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Platelet-dense (δ) granules are important for platelet function. Platelets contribute to host defense and vascular integrity during pneumonia and sepsis, and δ granule products, including adenosine diphosphate (ADP), can influence inflammatory responses. We therefore aimed to study the role of platelet δ granules in the host response during sepsis. Hermansky-Pudlak syndrome  (Hps)3coa  mice (with reduced δ granule content), mice treated with the platelet ADP receptor inhibitor clopidogrel, and appropriate control mice were infected with the human sepsis pathogen  Klebsiella pneumoniae  via the airways to induce pneumonia and sepsis. In order to override potential redundancy in platelet functions, we also studied  Hps3coa  and control mice with moderate antibody-induced thrombocytopenia (10%) prior to infection. We found that sepsis-induced thrombocytopenia tended to be less severe in  Hps3coa  mice, and was significantly ameliorated in  Hps3coa  mice with low pre-infection platelet counts. Bacterial growth was similar in  Hps3coa  and control mice in the presence of normal platelet counts prior to infection, but lower in the lungs of  Hps3coa  mice with low pre-infection platelet counts.  Hps3coa  mice had unaltered lung pathology and distant organ injury during pneumosepsis, irrespective of pre-infection platelet counts; lung bleeding did not differ between  Hps3coa  and control mice. Clopidogrel did not influence any host response parameter. These data suggest that platelet δ granules can play a detrimental role in pneumosepsis by aggravating thrombocytopenia and impairing local antibacterial defense, but that these unfavorable effects only become apparent in the presence of low platelet counts.

Platelet-Dense Granules Worsen Pre-Infection Thrombocytopenia during Gram-Negative Pneumonia-Derived Sepsis