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Interleukin-6 Protection in Hyperoxic Lung Injury^*

^* From the Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, CT.

Correspondence to: Nicholas S. Ward, MD, Pulmonary and Critical Care, Yale University, 333 Cedar St, New Haven, CT 06520

High concentrations of oxygen are well documented to cause lung injury. Interleukin-6 (IL-6) is a pleotropic cytokine that has been implicated in a variety of protective responses. To assess the effects of IL-6 in hyperoxic lung injury, transgene (+) mice, in which the Clara cell 10-kd protein (CC10) promoter drives the expression of human IL-6 in the airway, and transgene (-) littermate control mice were exposed to 100% oxygen to assess survival. Mice were assessed for BAL protein, membrane lipid peroxidation, and glutathione reductase activity. Transgene (-) mice exposed to 100% oxygen manifested severe lung injury with pulmonary edema and died 3 to 5 days after the initiation of the exposure. In contrast, transgene (+) animals manifested markedly enhanced survival, with 100% of the animals living for 8 days and the majority living beyond 10 days (p = 0.0001). Grossly, the lungs from transgene (-) animals exposed to 100% oxygen for 3 days appeared boggy and edematous. Similar alterations were not appreciated in the lungs of the transgene (+) animals. Three days of hyperoxia caused impressive increases in BAL protein in transgene (-) animals. This effect was markedly blunted in the transgene (+) animals (p = 0.0002). Pulmonary hemorrhage was also evident in the BAL fluid from the transgene (-) animals and to a much lesser extent in the transgene (+) animals. The levels of BAL leukocytes, however, were similar in both study populations. IL-6-induced protection in transgene (+) animals was also associated with a significant decrease in membrane lipid peroxidation; however, there were no significant differences in the levels of glutathione reductase activity. The targeted expression to IL-6 in the lung enhances tolerance to 100% oxygen while diminishing hyperoxia-induced pulmonary edema, alveolar hemorrhage, alveolar capillary protein leak, and lung lipid peroxidation. IL-6 may have therapeutic utility in the setting of hyperoxic lung injury.

This Article Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ward, N. S. Articles by Elias, J.A. Search for Related Content PubMed PubMed Citation Articles by Ward, N. S. Articles by Elias, J.A.