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1 as an Enhancer of Fas-Mediated Apoptosis of Lung Epithelial Cells
* Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; and
Research and Development Planning and Management Department, Mochida Pharmaceutical Company, Tokyo, Japan
Transforming growth factor-
1 (TGF-1) has important roles in
lung fibrosis and the potential to induce apoptosis in several types of
cells. We previously demonstrated that apoptosis of lung epithelial
cells induced by Fas ligation may be involved in the development of
pulmonary fibrosis. In this study, we show that TGF-1 induces
apoptosis of primary cultured bronchiolar epithelial cells via
caspase-3 activation and down-regulation of cyclin-dependent kinase
inhibitor p21. Concentrations of TGF-1 that were not sufficient to
induce apoptosis alone could enhance agonistic anti-Fas Ab or rFas
ligand-mediated apoptosis of cultured bronchiolar epithelial cells.
Soluble Fas ligand in the bronchoalveolar lavage fluid (BALF) from
patients with idiopathic pulmonary fibrosis (IPF) also induced
apoptosis of cultured bronchiolar epithelial cells that was
significantly attenuated by anti-TGF- Ab. Otherwise, BALF from
patients with hypersensitivity pneumonitis (HP) could not induce
apoptosis on bronchiolar epithelial cells, despite its comparable
amounts of soluble Fas ligand. The concentrations of TGF-1 in BALF
from patients with IPF were significantly higher compared with those in
BALF from patients with HP or controls. Furthermore, coincubation with
the low concentration of TGF-1 and HP BALF created proapoptotic
effects comparable with the IPF BALF. In vivo, the administration of
TGF-1 could enhance Fas-mediated epithelial cell apoptosis and lung
injury via caspase-3 activation in mice. Our results demonstrate a
novel role of TGF-1 in the pathophysiology of pulmonary fibrosis as
an enhancer of Fas-mediated apoptosis of lung epithelial
cells.
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