© 2003 American Thoracic Society DOI: 10.1165/rcmb.2002-0162OC Retrovirally Introduced Prostaglandin D2 Synthase Suppresses Lung Injury Induced by BleomycinDivision of Respiratory Internal Medicine, Department of Internal Medicine; Department of Microbiology; Division of Rheumatology, Department of Internal Medicine; and Department of Pharmacology, Kitasato University School of Medicine, Sagamihara-shi, Kanagawa; and Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki-shi, Kanagawa, Japan Address correspondence to: Izumi Hayashi, Department of Pharmacology, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan. E-mail: hayashii{at}med.kitasato-u.ac.jp
Hematopoietic prostaglandin D synthase (PGDS) is a key enzyme to produce prostaglandin (PG) D and J series. These PGs are involved in inflammation and immune system. The PGDS complementary DNA (cDNA)–expressing retrovirally transfected fibroblasts were introduced in vivo, and effect of the expression on lung injury induced by bleomycin was investigated in mice. Intravenous injection of PGDS cDNA-expressing fibroblasts significantly reduced lung edema, leukocyte infiltration in bronchoalveolar lavage (BAL) fluid, and pulmonary collagen content at 4 wk after instillation of bleomycin. Survival rate in mice instilled with the PGDS-expressing fibroblasts was higher than that in mice that received the mock transfection. Administration of 15-deoxy-
Abbreviations: basic fibroblast growth factor, bFGF • bronchoalveolar lavage, BAL • complementary DNA, cDNA • connective tissue growth factor, CTGF • cyclooxygenase, COX • 15-deoxy- This article has been cited by other articles:
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12,14-PGJ2, which is a nonenzymatic metabolite of PGD2, also attenuated the lung injury, suggesting mediation of PGs produced by PGDS for the attenuation. Introduction of PGDS cDNA-expressing fibroblasts suppressed expression of basic fibroblast growth factor, connective tissue growth factor, and collagen messenger RNAs in the lungs, as well as the levels of total proteins and hemoglobin in BAL fluid. These data suggest that the suppressive effect of PGDS on the lung injury could be partly mediated by edema formation and inhibition of genes involved in the fibrotic change. 
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