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American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 651-656, (2002)
© 2002 American Thoracic Society

Original Article

Tumor Necrosis Factor-{alpha} and Angiostatin Are Mediators of Endothelial Cytotoxicity in Bronchoalveolar Lavages of Patients with Acute Respiratory Distress Syndrome

Jürg Hamacher, Rudolf Lucas, H. Roger Lijnen, Susanne Buschke, Yves Dunant, Albrecht Wendel, Georges E. Grau, Peter M. Suter and Bara Ricou

Department of Anaesthesiology, Pharmacology, and Surgical Intensive Care, University Medical Center, Geneva, Switzerland; Division of Biochemical Pharmacology, University of Konstanz, Konstanz, Germany; Cardiovascular Research, VIB, University of Leuven, Leuven, Belgium; and Department of Physiology, Université de la Méditerranée, Marseille, France

Correspondence and requests for reprints should be addressed to Rudolf Lucas, Ph.D., Biochemical Pharmacology, Department of Biology, Universitätsstrasse 10, Box M668, D-78457 Konstanz, Germany. E-mail: rudolf.lucas{at}uni-konstanz.de

Acute respiratory distress syndrome (ARDS) is characterized by an extensive alveolar capillary leak, permitting contact between intra-alveolar factors and the endothelium. To investigate whether factors contained in the alveolar milieu induce cell death in human lung microvascular endothelial cells, we exposed these cells in vitro to bronchoalveolar lavage fluid (BALF) supernatants from control patients, patients at risk of developing ARDS, and patients with early- and late-phase ARDS. In contrast to BALF from control patients, a significant cytotoxicity was found in BALF from patients at risk of developing ARDS, with late-phase ARDS, and especially from patients with early-phase ARDS. Subsequently, we determined the levels of factors known to exert cytotoxicity in endothelial cells, i.e., tumor necrosis factor (TNF)-{alpha}, transforming growth factor (TGF)-ß1, and angiostatin. BALF from patients at risk of developing ARDS, with early-phase ARDS, and with late-phase ARDS, contained increased levels of TNF-{alpha} and angiostatin, but not of TGF-ß1, as compared with BALF from control patients. Whereas inhibition of TGF-ß1 had no effect in this setting, neutralization of TNF-{alpha} or angiostatin inhibited the cytotoxic activity on endothelial cells of part of the early-phase ARDS BALF. These results indicate that TNF-{alpha} and angiostatin may contribute to ARDS-related endothelial injury.

Key Words: respiratory distress syndrome • cytotoxicity • endothelium




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