Low levels of interleukin-10 in patients with transfusion-related acute lung injury

Transfusion related acute lung injury (TRALI) is the leading cause of transfusion-related fatalities (FDA Report 2016) (1) and is characterized by the acute onset of respiratory distress within 6 hours following blood transfusion (2,3). The clinical diagnosis is confirmed in case of newly developing acute respiratory distress: PaO<₂/FiO₂ ratio (ratio of arterial oxygen partial pressure to fractional inspired oxygen) <300 mmHg or arterial oxygen saturation <90% at room air; newly developed or worsened bilateral pulmonary infiltrates indicative of pulmonary edema on chest X-ray; emergence of all symptoms within 6 hours upon blood transfusion and exclusion of cardiac ischemia and transfusion associated circulatory overload (TACO). Apart from supportive measures, such as oxygen or ventilation, no specific therapies are available. The pathogenesis is incompletely understood, however, a two-hit model is usually assumed to underlie the disease pathology. The first hit consists of a pre-disposing factor present in the recipient such as inflammation while the second hit is conveyed by factors present in the transfused blood product such as anti-leukocyte antibodies (3). For example, the acute phase protein C-reactive protein (CRP) which rapidly increases during infection and inflammation was shown to enhance antibody-mediated TRALI in mice (4) and in line with that data, CRP was found to be elevated in human TRALI patients (5) confirming its role as a first hit risk factor in human TRALI.