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Research Article Free access | 10.1172/JCI117630

Chemokine expression during hepatic ischemia/reperfusion-induced lung injury in the rat. The role of epithelial neutrophil activating protein.

L M Colletti, S L Kunkel, A Walz, M D Burdick, R G Kunkel, C A Wilke, and R M Strieter

Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor 48109-0360.

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Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor 48109-0360.

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Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor 48109-0360.

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Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor 48109-0360.

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Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor 48109-0360.

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Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor 48109-0360.

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Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor 48109-0360.

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Published January 1, 1995 - More info

Published in Volume 95, Issue 1 on January 1, 1995
J Clin Invest. 1995;95(1):134–141. https://doi.org/10.1172/JCI117630.
© 1995 The American Society for Clinical Investigation
Published January 1, 1995 - Version history
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Abstract

The liver is highly susceptible to a number of pathological insults, including ischemia/reperfusion injury. One of the striking consequences of liver injury is the associated pulmonary dysfunction that may be related to the release of hepatic-derived cytokines. We have previously employed an animal model of hepatic ischemia/reperfusion injury, and demonstrated that this injury causes the production and release of hepatic-derived TNF, which mediates a neutrophil-dependent pulmonary microvascular injury. In this study, we have extended these previous observations to assess whether an interrelationship between TNF and the neutrophil chemoattractant/activating factor, epithelial neutrophil activating protein-78 (ENA-78), exists that may be accountable for the pathology of lung injury found in this model. In the context of hepatic ischemia/reperfusion injury, we demonstrated the following alterations in lung pathophysiology: (a) an increase in pulmonary microvascular permeability, lung neutrophil sequestration, and production of pulmonary-derived ENA-78; (b) passive immunization with neutralizing TNF antiserum resulted in a significant suppression of pulmonary-derived ENA-78; and (c) passive immunization with neutralizing ENA-78 antiserum resulted in a significant attenuation of pulmonary neutrophil sequestration and microvascular permeability similar to our previous studies with anti-TNF. These findings support the notion that pulmonary ENA-78 produced in response to hepatic-derived TNF is an important mediator of lung injury.

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