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Babu V. Naidu
Steven M. Woolley
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Right arrow Lung - transplantation

J Thorac Cardiovasc Surg 2004;127:1502-1508
© 2004 The American Association for Thoracic Surgery

Cardiothoracic transplantation

Early tumor necrosis factor-{alpha} release from the pulmonary macrophage in lung ischemia-reperfusion injury

Babu V. Naidu, FRCSa, Steven M. Woolley, MRCSa, Alexander S. Farivar, MDa, Robert Thomas, BAa, Charles H. Fraga, MSa, Christopher H. Goss, MD, MS, FCCPb, Michael S. Mulligan, MD, FACSa,*

a Division of Cardiothoracic Surgery, Department of Surgery, University of Washington Medical Center, Seattle, Wash, USA
b Division of Pulmonary Medicine, University of Washington Medical Center, Seattle, Wash, USA

Received for publication February 27, 2003; revisions received August 4, 2003; accepted for publication August 18, 2003.

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

OBJECTIVE: Tumor necrosis factor-{alpha} is a proinflammatory mediator required for the development of experimental lung ischemia-reperfusion injury. The alveolar macrophage is a rich source of tumor necrosis factor-{alpha} in multiple models of acute lung injury. The present study was undertaken to determine whether the alveolar macrophage is an important source of tumor necrosis factor-{alpha} in lung ischemia-reperfusion injury and whether suppression of its function protects against injury.

METHODS: Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours. Treated animals received gadolinium chloride, a rare earth metal that inhibits macrophage function. Injury was quantitated via lung tissue neutrophil accumulation (myeloperoxidase content), lung vascular permeability, and bronchoalveolar lavage fluid leukocyte, cytokine, and chemokine content. Separate samples were generated for immunohistochemistry.

RESULTS: Tumor necrosis factor-{alpha} secretion occurred at 15 minutes of reperfusion and was localized to the alveolar macrophage by immunohistochemistry. In gadolinium-treated animals, lung vascular permeability was reduced by 66% at 15 minutes (P < .03) of reperfusion and by 34% at 4 hours (P < .02) of reperfusion. Suppression of macrophage function resulted in a 35% reduction in lung myeloperoxidase content (P < .03) and similar reductions in bronchoalveolar lavage leukocyte accumulation. Tumor necrosis factor-{alpha} and microphage inflammatory protein-1{alpha} protein levels were markedly reduced in the bronchoalveolar lavage of gadolinium-treated animals by enzyme-linked immunosorbent assay.

CONCLUSIONS: The alveolar macrophage secretes tumor necrosis factor-{alpha} protein by 15 minutes of reperfusion, which orchestrates the early events that eventually result in lung ischemia-reperfusion injury at 4 hours. Gadolinium pretreatment markedly reduces tumor necrosis factor-{alpha} elaboration, resulting in significant protection against lung ischemia-reperfusion injury.




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