Abstract
Primary Graft Dysfunction (PGD) after lung transplantation is the result of ischemia-reperfusion (I-R) injury. Abnormal activation of innate immunity, in response to I-R injury, mediated by Toll-like receptors and interleukin-1 induced long pentraxin-3 (PTX3) release leading to complement activation may play a role in PGD pathogenesis. We hypothesized that elevated PTX3 levels are associated with PGD.
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