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The Journal of Immunology, 2005, 175: 6931-6939.
Copyright © 2005 by The American Association of Immunologists

CXCR2/CXCR2 Ligand Biology during Lung Transplant Ischemia-Reperfusion Injury1

John A. Belperio2,*, Michael P. Keane*, Marie D. Burdick*, Brigitte N. Gomperts{dagger}, Ying Ying Xue*, Kurt Hong{ddagger}, Javier Mestas*, David Zisman*, Abbas Ardehali§, Rajan Saggar*, Joseph P. Lynch, III*, David J. Ross* and Robert M. Strieter*,{dagger},¶

* Department of Medicine, Division of Pulmonary and Critical Care Medicine, {dagger} Department of Pediatrics, {ddagger} Department of Nutrition, § Department of Surgery, and Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095

Lung transplantation is a therapeutic option for a number of end-stage pulmonary disorders. Early lung allograft dysfunction (ischemia-reperfusion injury) continues to be the most common cause of early mortality after lung transplantation and a significant risk factor for the development of bronchiolitis obliterans syndrome. Ischemia-reperfusion injury is characterized histopathologically by lung edema and a neutrophil predominate leukocyte extravasation. The specific mechanism(s) that recruit leukocytes to the lung during post-lung transplantation ischemia-reperfusion injury have not been fully elucidated. Because the ELR+ CXC chemokines are potent neutrophil chemoattractants, we investigated their role during post-lung transplantation ischemic-reperfusion injury. We found elevated levels of multiple ELR+ CXC chemokines in human bronchoalveolar lavage fluid from patients with ischemia-reperfusion injury. Proof of concept studies using a rat orthotopic lung transplantation model of "cold" ischemic-reperfusion injury demonstrated an increase in lung graft neutrophil sequestration and injury. In addition, lung expression of CXCL1, CXCL2/3, and their shared receptor CXCR2 paralleled lung neutrophil infiltration and injury. Importantly, inhibition of CXCR2/CXCR2 ligand interactions in vivo led to a marked reduction in lung neutrophil sequestration and graft injury. Taken together these experiments support the notion that increased expression of ELR+ CXC chemokines and their interaction with CXCR2 plays an important role in the pathogenesis of post-lung transplantation cold ischemia-reperfusion injury.


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