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Published ahead of print on September 22, 2005, doi:10.1165/rcmb.2005-0068OC

Am. J. Respir. Cell Mol. Biol., Volume 34, Number 1, January 2006, 101-107

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Submitted on February 15, 2005
Revised on September 21, 2005

Leukotriene C4 Induces TGF-{beta}1 Production in Airway Epithelium via p38 Kinase Pathway

Diahn-Warng Perng1*, Yu-Chung Wu2, Kuo-Ting Chang3, Mo-Tzu Wu4, Yih-Chy Chiou5, Kang-Cheng Su4, Reury-Perng Perng1, and Yu-Chin Lee1

1 Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; School of Medicine, National Yang-Ming University, Taipei, Taiwan, 2 Division of Chest Surgery, Taipei Veterans General Hospital, Taipei, Taiwan; School of Medicine, National Yang-Ming University, Taipei, Taiwan, 3 Division of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli County, Taiwan, 4 Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, 5 School of Medical Technology and Engineering, National Yang-Ming University, Taipei, Taiwan

* To whom correspondence should be addressed. E-mail: dwperng{at}vghtpe.gov.tw.

Cysteinyl leukotrienes (CysLTs) play an important role in the pathogenesis of airway remodeling. We investigated the interaction between epithelium and CysLTC4, and the contribution of this interaction to airway fibrosis. Human airway epithelial cells were grown on air-liquid interface culture inserts. CysLTC4 was employed to stimulate the cells. Conditioned medium following CysLTC4 stimulation was co-incubated with human lung fibroblasts. Our results have demonstrated that CysLTC4 stimulates airway epithelial cells, through a p38 mitogen-activated protein kinase (MAPK) activation mechanism, to produce transforming growth factor {beta}1 (TGF-{beta}1), which results in fibroblast proliferation. The selective p38 MAPK inhibitor S203580 successfully inhibits p38 MAPK phosphorylation and subsequent TGF-{beta}1 production. CysLT1 receptor antagonist montelukast and corticosteroid inhibit TGF-{beta}1 production at the mRNA and protein levels. When treated with LTC4, the conditioned medium from epithelial cells enhances fibroblast proliferation, this mitogenic effect being attributed to TGF-{beta}1 and LTC4 remaining in the culture medium. In addition, LTC4 itself acts as a potential growth factor for lung fibroblasts. These data indicate that interactions between LTC4 and airway epithelial cells may contribute to the pathogenesis of airway remodeling. Early intervention to stop these processes may be useful in preventing airway fibrosis in chronic allergic inflammation.




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