Transfusion-related acute lung injury (
TRALI) is the leading cause of transfusion-associated morbidity and mortality. Activated platelets have important roles in
TRALI and CD62P was identified to be an important
indicator of platelet activation. However, the precise roles of CD62P in
TRALI have remained elusive. The present study assessed CD62P accumulation during storage of
apheresis platelet concentrates (A‑Plts) and established a mouse model of
TRALI to further investigate the roles of CD62P in
TRALI. The results showed that the CD62P concentration in A‑Plts was increased with the storage time. Mice were treated with monoclonal major histocompatibility complex (MHC)‑1 antibody to induce
TRALI. The murine model of
TRALI was successfully established as evidenced by pulmonary oedema, accompanied by decreased clearance of bronchoalveolar lavage fluid (BALF), increased pulmonary and systemic
inflammation, elevated lung
myeloperoxidase (MPO) activity as well as increased pulmonary and systemic coagulation in the
TRALI group compared with those in the control group. To further determine the role of CD62P in
TRALI, mice were treated with anti‑CD62P antibody to knockdown CD62P in vivo. It was found that pulmonary oedema, BALF clearance, pulmonary and systemic
inflammation, MPO activity as well as pulmonary and systemic coagulation were decreased in the
TRALI + anti‑CD62P antibody group compared with those in the
TRALI + isotype antibody group. The present study supported the notion that CD62P is involved in mediating
TRALI and may provide an important molecular basis for enhancing the clinical safety and effectiveness of
platelet transfusion.