TY - JOUR
T1 - Interferon-γ inhibits the growth of human bronchial epithelial cells independently of transforming growth factor-β-1 and nitric oxide (NO)
AU - Kobayashi, Masato
AU - Niitsuma, Tomoyuki
AU - Hayashi, Torhu
AU - Tanaka, Mitsuru
AU - Takizawa, Hajime
N1 - Funding Information:
This work was supported in part by the Grant from Adult Diseases Memorial Foundation, from the Ministry of Education, Science and Culture, and Manabe Medical Foundation.
PY - 1998/3/6
Y1 - 1998/3/6
N2 - It has been emphasized that epithelial injury is closely correlated with airway hyperresponsiveness, which is one of the important pathophysiological characteristics of bronchial asthma. Growth of epithelial cells is important in the mucosal repair processes and is believed to be regulated by growth factors produced by inflammatory and immune effector cells as well as epithelial cells themselves. We studied the role of T cell-derived lymphokines IFNγ and IL-4 on the proliferation of human bronchial epithelial cell line BEAS-2B, IFNγ, but not IL-4, showed a dose-dependent growth inhibitory activity in vitro. Its activity was via its specific receptors on the cells, was augmented by TNFα, and was independent of the activity of endogenous TGFβ and nitric oxide. These results suggested that Th-1 T cells-derived lymphokine IFNγ might be involved in the repair processes after mucosal injury found in bronchial asthma.
AB - It has been emphasized that epithelial injury is closely correlated with airway hyperresponsiveness, which is one of the important pathophysiological characteristics of bronchial asthma. Growth of epithelial cells is important in the mucosal repair processes and is believed to be regulated by growth factors produced by inflammatory and immune effector cells as well as epithelial cells themselves. We studied the role of T cell-derived lymphokines IFNγ and IL-4 on the proliferation of human bronchial epithelial cell line BEAS-2B, IFNγ, but not IL-4, showed a dose-dependent growth inhibitory activity in vitro. Its activity was via its specific receptors on the cells, was augmented by TNFα, and was independent of the activity of endogenous TGFβ and nitric oxide. These results suggested that Th-1 T cells-derived lymphokine IFNγ might be involved in the repair processes after mucosal injury found in bronchial asthma.
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U2 - 10.1006/bbrc.1998.8223
DO - 10.1006/bbrc.1998.8223
M3 - Article
C2 - 9514890
AN - SCOPUS:0032489231
SN - 0006-291X
VL - 244
SP - 126
EP - 130
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -