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Interleukin-6 Protection in Hyperoxic Lung Injury* FREE TO VIEW

Nicholas S. Ward, MD; A.B. Waxman, MD, FCCP; O. Einarsson, MD; J.A. Elias, MD
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*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

Chest. 1999;116(suppl_1):26S. doi:10.1378/chest.116.suppl_1.26S
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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.




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