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Right arrow Lung - transplantation

J Thorac Cardiovasc Surg 2003;126:200-207
© 2003 The American Association for Thoracic Surgery

Cardiothoracic transplantation

Early activation of the alveolar macrophage is critical to the development of lung ischemia-reperfusion injury

Babu V. Naidu, FRCSa, Baiya Krishnadasan, MDa, Alexander S. Farivar, MDa, Steven M. Woolley, MRCSa, Robert Thomas, BAa, Nico Van Rooijen, PhDb, Edward D. Verrier, MDa, Michael S. Mulligan, MDa,*

a Division of Cardiothoracic Surgery,a Department of Surgery, University of Washington, Seattle, Wash,USA
b Department of Cell Biology and Immunology,b Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands

Received for publication May 31, 2002; accepted for publication December 4, 2002.

* Address for reprints: Michael S. Mulligan, MD, Box 356310, University of Washington, 1959 NE Pacific St, Seattle, WA 98195, USA
msmmd{at}u.washington.edu

OBJECTIVES: Activation of the alveolar macrophage is critical to the development of nonischemic inflammatory lung injury. The present studies were undertaken to determine whether the alveolar macrophage plays a similarly important role in lung ischemia-reperfusion injury.

METHODS: The left lungs of male rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours. Treated animals received liposome-encapsulated clodronate, which depletes alveolar macrophages. Injury was quantitated in terms of vascular permeability, tissue neutrophil accumulation, and bronchoalveolar lavage fluid leukocyte, chemokine, and cytokine content. Lung homogenates were also analyzed for nuclear translocation of the transcription factors nuclear factor {kappa}B and activator of protein 1.

RESULTS: Depletion of alveolar macrophages reduced lung vascular permeability by 53% compared with that seen in control animals (permeability indices: 0.88 ± 0.07 to 0.46 ± 0.04, P < .001). The protective effects of alveolar macrophage depletion correlated with a 50% reduction in tissue myeloperoxidase content (0.62 ± 0.07 to 0.33 ± 0.03, P < .006) and marked reductions in bronchoalveolar lavage fluid leukocyte accumulation. Alveolar macrophage–depleted animals also demonstrated marked reductions of the elaboration of multiple proinflammatory chemokines and cytokines in the lavage effluent and nuclear transcription factors in lung homogenates.

CONCLUSION: It is likely that the alveolar macrophage is the key early source of multiple proinflammatory mediators that orchestrate lung ischemia-reperfusion injury. Depleting alveolar macrophages is protective against injury, supporting its central role in oxidant stress–induced cytokine and chemokine release and the subsequent development of lung injury.




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