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Am J Physiol Lung Cell Mol Physiol (October 8, 2004). doi:10.1152/ajplung.00016.2004
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Submitted on January 20, 2004
Accepted on October 5, 2004

Protective Effect of IL-6 On The Alveolar Epithelial Cell Death Induced By Hydrogen Peroxide

Hiroshi Kida1, Mitsuhiro Yoshida2*, Shigenori Hoshino2, Koji Inoue2, Yukihiro Yano2, Masahiko Yanagita2, Toru Kumagai2, Tadashi Osaki2, Isao Tachibana2, Yukihiko Saeki1, and Ichiro Kawase1

1 National Hospital Organization, Japan, Osaka Minami Medical Center, Kawachinagano, Osaka, Japan
2 Department of Molecular Medicine, Osaka university, Suita, Osaka, Japan

* To whom correspondence should be addressed. E-mail: hiroinosaka{at}hotmail.com.

The goal of this study was to examine whether IL-6 could directly protect lung resident cells, especially alveolar epithelial cells, from reactive oxygen species (ROS)-induced cell death. ROS induced IL-6 gene expression in organotypic lung slices of wild type mice (WT). ROS also induced IL-6 gene expression in mouse primary lung fibroblasts, dose-dependently. The organotypic lung slices of WT were more resistant to ROS-induced DNA fragmentation than those of IL-6 deficient mice (IL-6 -/-). WT resistance against ROS was abrogated by treatment with anti-IL-6 antibody. Terminal deoxynucleotidyltransferase (TdT)-mediated dUTP nick end labeling (TUNEL) stain and electron microscopy revealed that DNA fragmented cells in the IL-6 -/- slice included alveolar epithelial cells and endothelial cells. In vitro studies demonstrated that IL-6 reduced ROS-induced A549 alveolar epithelial cell death. Taken together, these data suggest that IL-6 played an anti-oxidant role in the lung by protecting lung resident cells, especially alveolar epithelial cells, from ROS-induced cell death.




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