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Targeted Lung Expression of Interleukin-11 Enhances Murine Tolerance of 100% Oxygen and Diminishes Hyperoxia-Induced DNA Fragmentation* FREE TO VIEW

A. B. Waxman, MD, PhD; O. Einarsson; T. Seres; R. G. Knickelbein; R. Homer; J. B. Warshaw; R. Johnston; J. A. Elias
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*From Yale University School of Medicine, New Haven, CT.

Correspondence to: A. B. Waxman, MD, PhD, Yale University School of Medicine, 333 Cedar St, PO Box 208057, New Haven, CT 06520

Chest. 1999;116(suppl_1):8S-9S. doi:10.1378/chest.116.suppl_1.8S
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Acute lung injury is a frequent and treatment-limiting consequence of therapy with hyperoxic gas mixtures. To determine if interleukin-11 (IL-11) is protective in oxygen (O2) toxicity, we compared the effects of 100% O2 on transgenic mice that overexpress IL-11 in the lung and transgene (−) control mice. IL-11 markedly enhanced survival in 100% O2 with 100% of transgene (−) animals dying within 72 to 96 h and >90% of transgene (+) animals surviving for >10 days. This protection was associated with markedly diminished alveolar-capillary protein leak, endothelial and epithelial membrane injury, lipid peroxidation, and pulmonary neutrophil recruitment. Significant differences in copper zinc superoxide dismutase and catalase activities were not noted and the levels of total, reduced, and oxidized glutathione were similar in transgene (+) and (−) animals. Glutathione reductase, glutathione peroxidase, and manganese superoxide dismutase activities were slightly higher in transgene (+) as vs (−) mice after 100% O2 exposure, and IL-11 diminished hyperoxia-induced expression of IL-1 and tumor necrosis factor. Hyperoxia also caused cell death with DNA fragmentation in the lungs of transgene (−) animals and IL-11 markedly diminished this cell death response. These studies demonstrate that IL-11 markedly diminishes hyperoxic lung injury. They also demonstrate that this protection is associated with small changes in lung antioxidants, diminished hyperoxia-induced IL-1 and tumor necrosis factor production, and markedly suppressed hyperoxia-induced DNA fragmentation.




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