Non-Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

Nonclassical Monocytes Promote Edema in Lung Allografts from Traumatic Brain Injury Donors.

Abstract

Head trauma remains one of the most common causes of brain death among human lung donors. Unfortunately, traumatic brain injury (TBI)-associated lung dysfunction precludes a large proportion of such lung donor offers from clinical transplantation (1). Even those lungs from TBI donors with acceptable gas exchange prior to transplantation demonstrate increased susceptibility for primary graft dysfunction, the predominant cause of early post–lung transplant mortality. However, the mechanisms through which TBI leads to donor lung injury and subsequent primary graft dysfunction remain unclear (2). In this letter, we report that immunological mechanisms driven by intravascular CCR22 nonclassical monocytes (NCM) may play a role in the pathogenesis of pulmonary edema associated with TBI. Using our previously validated murine model of TBI