Non-Hemostatic Platelet-Dependent Protection Against Murine Bacterial Pneumonia

Platelets can recognize and destroy microbial pathogens through the release of antimicrobial proteins, suggesting that they may contribute to innate immune defense against infection.

To determine whether platelets contribute to pulmonary innate immunity during bacterial pneumonia and to distinguish their antimicrobial functions from their hemostatic role.

Mice were exposed to aerosolized Gram-negative Pseudomonas aeruginosa or Gram-positive Streptococcus pneumoniae. Platelet number or function was reduced by antibody-mediated platelet depletion, thrombopoietin gene deletion, or aspirin treatment. Clinical outcomes, mortality, pulmonary pathogen burden, and lung histopathology were assessed.

Thrombocytopenic and aspirin-treated mice had increased mortality following bacterial pneumonia. Lung congestion and pathogen burden increased in proportion to the severity of thrombocytopenia. In contrast, pulmonary hemorrhage was observed only in severely thrombocytopenic mice, indicating that impaired antimicrobial defense occurred at platelet levels sufficient to maintain hemostasis.

Platelets actively protect against both Gram-negative and Gram-positive bacterial pneumonia. This protective effect is distinct from their hemostatic function: platelets contribute directly to antimicrobial host defense, whereas their hemostatic activity maintains a physical barrier that limits local pathogen spread.