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-Galactosylceramide Attenuates the Development of Bleomycin-Induced Pulmonary Fibrosis
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Departments of
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Respiratory Medicine, and
Immunology, University of Tsukuba, Tsukuba, Japan;
Laboratory for Immune Receptor, RIKEN Research Center for Allergy and Immunology, Tsukuba, Japan;
Precursory Research for Embryonic Science and Technology Office, Japan Science and Technology, Kawaguchi, Japan;
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Laboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan; and
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Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan
Pulmonary fibrosis is an end-stage disorder for which efficacious therapeutic options are not readily available. Although its pathogenesis is poorly understood, pulmonary fibrosis occurs as a result of various inflammations. NKT cells modulate inflammation because of their ability to produce large amounts of cytokines by stimulation with their glycolipid ligand. In the present study, we investigated the effects of 
-galactosylceramide (-GalCer), a selective NKT cell ligand, on the development of bleomycin-induced pulmonary fibrosis. Treatment of mice with -GalCer prolonged their survival under bleomycin administration by attenuating the development of pulmonary fibrosis. The protective effects of -GalCer were associated with an increase in the pulmonary level of IFN-
and a decrease in the pulmonary level of fibrogenic cytokines such as TGF-
and connective tissue growth factor. The initial pulmonary inflammation caused by bleomycin was also attenuated by -GalCer with the reduction of the macrophage inflammatory protein-2 level. The protective effects of -GalCer were markedly reduced in mice lacking NKT cells or as a result of treatment with anti-IFN- Ab. These results suggest that -GalCer suppresses bleomycin-induced acute pulmonary inflammation and thus attenuates the development of pulmonary fibrosis possibly by regulating several cytokine levels.
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