During TRALI, which chemotactic factor is primarily responsible for pulmonary leukosequestration?

In the context of Transfusion-Related Acute Lung Injury (TRALI), the primary chemotactic factor responsible for pulmonary leukosequestration is C5a. C5a is a potent anaphylatoxin generated during the complement activation process and plays a critical role in the inflammatory response.

When TRALI occurs, antibodies present in the transfused blood product activate the complement cascade, leading to the generation of C5a. This molecule promotes the attraction of neutrophils to the pulmonary vasculature, where they aggregate, becoming sequestered in the lungs. The accumulation of these leukocytes results in tissue damage, vascular permeability, and subsequent clinical manifestations of lung injury.

C5a’s ability to enhance adhesion molecule expression on neutrophils and vascular endothelial cells further underscores its significance in leukocyte recruitment and accumulation during TRALI. While other chemotactic factors like FMLP, IL-8, and Leukotriene B4 are involved in the inflammatory response, C5a is uniquely activated by the complement system in this specific context, highlighting its central role in the pathophysiology of TRALI.