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This Article Full Text Full Text (PDF) All Versions of this Article: 288/2/L342    most recent 00016.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (13) Citing Articles via Google Scholar Google Scholar Articles by Kida, H. Articles by Kawase, I. Search for Related Content PubMed PubMed Citation Articles by Kida, H. Articles by Kawase, I.

Protective effect of IL-6 on alveolar epithelial cell death induced by hydrogen peroxide

¹National Hospital Organization Japan, Osaka Minami Medical Center, Kawachinagano, Osaka; and ²Department of Molecular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

Submitted 20 January 2004 ; accepted in final form 5 October 2004

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 (WT) mice. 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 (IL-6–/–) mice. WT resistance against ROS was abrogated by treatment with anti-IL-6 antibody. TdT-mediated dUTP nick end labeling 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. Together, these data suggest that IL-6 played an antioxidant role in the lung by protecting lung resident cells, especially alveolar epithelial cells, from ROS-induced cell death.

lung slice culture; oxidative stress; diffuse alveolar damage; apoptosis; interleukin-6

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