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Am J Physiol Lung Cell Mol Physiol 291: L1018-L1026, 2006. First published July 21, 2006; doi:10.1152/ajplung.00086.2006
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Alveolar macrophage activation is a key initiation signal for acute lung ischemia-reperfusion injury

Minqing Zhao,1 Lucas G. Fernandez,1 Allan Doctor,2 Ashish K. Sharma,1 Alexander Zarbock,3 Curtis G. Tribble,1 Irving L. Kron,1 and Victor E. Laubach1

Departments of 1Surgery and 2Pediatrics, and the 3Cardiovascular Research Center, University of Virginia Health System, Charlottesville, Virginia

Submitted 9 March 2006 ; accepted in final form 13 July 2006

Lung ischemia-reperfusion (I/R) injury is a biphasic inflammatory process. Previous studies indicate that the later phase is neutrophil-dependent and that alveolar macrophages (AMs) likely contribute to the acute phase of lung I/R injury. However, the mechanism is unclear. AMs become activated and produce various cytokines and chemokines in many inflammatory responses, including transplantation. We hypothesize that AMs respond to I/R by producing key cytokines and chemokines and that depletion of AMs would reduce cytokine/chemokine expression and lung injury after I/R. To test this, using a buffer-perfused, isolated mouse lung model, we studied the impact of AM depletion by liposome-clodronate on I/R-induced lung dysfunction/injury and expression of cytokines/chemokines. I/R caused a significant increase in pulmonary artery pressure, wet-to-dry weight ratio, vascular permeability, tumor necrosis factor (TNF)-{alpha}, monocyte chemoattractant protein (MCP)-1, and macrophage inflammatory protein (MIP)-2 expression, as well as decreased pulmonary compliance, when compared with sham lungs. After AM depletion, the changes in each of these parameters between I/R and sham groups were significantly attenuated. Thus AM depletion protects the lungs from I/R-induced dysfunction and injury and significantly reduces cytokine/chemokine production. Protein expression of TNF-{alpha} and MCP-1 are positively correlated to I/R-induced lung injury, and AMs are a major producer/initiator of TNF-{alpha}, MCP-1, and MIP-2. We conclude that AMs are an essential player in the initiation of acute lung I/R injury.

pulmonary transplantation; clodronate; inflammation; chemokines


Address for reprint requests and other correspondence: M. Zhao, Dept. of Surgery, Univ. of Virginia Health System, P.O. Box 801359, Charlottesville, VA 22908 (e-mail: mz2v{at}virginia.edu)




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