Interleukin-1Î² increases airway epithelial cell mitogenesis partly by stimulating endothelin-1 production
To investigate the influence of interleukin-1Î² (IL-1Î²) on airway epithelial cell growth, we measured [3H]thymidine incorporation and cell numbers of cultured porcine tracheal epithelial cells in the presence or absence of human recombinant IL-1Î² with or without the following: goat antiporcine polyclonal antibody to platelet-derived growth factor (PDGF); IL- 1 receptor antagonist; indomethacin; PD-145065, a combined endothelin-A and - B receptor antagonist; BQ-123, an antagonist selective for endothelin-A receptors; or phosphoramidon, an inhibitor, in part, of endothelin-converting enzymes, including neutral endopeptidase. We found that IL-1Î² stimulated the proliferation of airway epithelial cells, and this response was inhibited by the IL-1 receptor antagonist and by PD-145065 or BQ-123. However, neither indomethacin nor PDGF antibody was influential. The endothelin receptor antagonists also decreased basal thymidine incorporation by these cells as did phosphormidon, although to a lesser degree. Data from radioimmunoassays indicated that phosphormidon reduced the endogenous production of endothelin- 1 from the cells, and IL-1Î² clearly increased it over time. We conclude that IL-1Î² is a stimulant of airway epithelial cell growth, and its mitogenic effects are mediated, in part, by endogenous endothelin-1 production.
Murlas, C. G.; Sharma, Avadhesh C.; Gulati, A.; and Najmabadi, F., "Interleukin-1Î² increases airway epithelial cell mitogenesis partly by stimulating endothelin-1 production" (1997). PCOM Scholarly Papers. 950.