Key features of the underlying pathophysiology of Transfusion-related acute lung injury

Transfusion-related acute lung injury (TRALI) remains a leading cause of blood transfusion associated mortality, particularly in the intensive care unit. TRALI is underrecognized, underreported and lacks specific biomarkers and clinical therapies.

In this review, the focus will be on the key pathophysiological features of TRALI. This will include the latest insights into the critical importance of complement (in contrast to Fcγ-receptors; FcγRs) as a driver of TRALI, and the role of recipient immune cells such as neutrophils and macrophages, and also the contribution of the pulmonary endothelium.

Increased efforts are needed to stimulate active reporting of TRALI cases. More research into the immuno-cellular pathophysiology of TRALI is required, including the role of the pulmonary endothelium. Heterogeneity in the underlying clinical condition and the different transfusion triggers should be taken into consideration. This will aid in the search for novel biomarkers and therapeutic modalities. At the moment, the most promising potential therapeutic strategies appear to be administration of interleukin (IL)-10, inhibition of complement activation and blockade of Osteopontin (OPN). Follow-up investigations are, however, highly warranted which should pave the way for multicenter international clinical trials, in order to battle the mortality due to TRALI.