title: Accumulation of CD62P during storage of apheresis platelet concentrates and the role of CD62P in transfusion-related acute lung injury.
abstract: 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.
authors.affiliation: Department of Blood Transfusion, The General Hospital of The People's Liberation Army, Beijing 100085, P.R. China.
authors.forename: Shan
authors.initials: S
authors.lastname: Tong
authors.affiliation: Department of Blood Transfusion, The General Hospital of The People's Liberation Army, Beijing 100085, P.R. China.
authors.forename: Haibao
authors.initials: H
authors.lastname: Wang
authors.affiliation: Department of Blood Transfusion, The General Hospital of The People's Liberation Army, Beijing 100085, P.R. China.
authors.forename: Ting
authors.initials: T
authors.lastname: Zhang
authors.affiliation: Department of Blood Transfusion, The General Hospital of The People's Liberation Army, Beijing 100085, P.R. China.
authors.forename: Linfeng
authors.initials: L
authors.lastname: Chen
authors.affiliation: Department of Blood Transfusion, The General Hospital of The People's Liberation Army, Beijing 100085, P.R. China.
authors.forename: Bowei
authors.initials: B
authors.lastname: Liu
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology* / Q000276:immunology / Q000473:pathology*; D000818:Animals; D001792:Blood Platelets / Q000276:immunology / Q000473:pathology*; D001793:Blood Preservation; D016207:Cytokines / Q000097:blood / Q000276:immunology; D008168:Lung / Q000276:immunology / Q000473:pathology*; D008297:Male; D008807:Mice, Inbred BALB C; D019007:P-Selectin / Q000032:analysis* / Q000276:immunology; D009195:Peroxidase / Q000276:immunology; D015539:Platelet Activation; D017713:Platelet Transfusion / Q000009:adverse effects*
chemical_list: D016207:Cytokines; D019007:P-Selectin; D009195:Peroxidase