Cigarette Smoke Extract Stimulates IL15 Expression in Human Lung Carcinoma Cells

Abstract

P-276 Abstract: Cigarette smoke is one of the major environmental air pollutants causes various airway injuries and diseases. The toxicity of cigarette smoke can directly lead the cells into apoptosis via the suppression of the gene expression. One of the by-products of cigarette smoke, reactive oxygen species (ROS), causes the oxidative damage and the repair process out of function in inflammatory cells. This study was to confer the dose and time course of cigarette smoke extract (CSE) effect on the expression of interleukin-15 (IL-15) in human airway epithelial carcinoma cells. Cigarette smoke extract was prepared from mainstream smoke of cigarettes, were withdrawn steadily via a peristaltic pump through a vessel of containing culture medium. Human mucoepidermoid pulmonary carcinoma cells (NCI-H292) were treated respectively with 10%-, 30%- and 50%-CSE for one or 3 hours exposure (high dose and short-term exposure), and 1.25%-, 2.5%- and 5%-CSE for 24 hours exposure (low dose and long-term exposure). The live and dead assay is measured for cell viability. Total RNA were harvested from treated NCI-H292 cells to determine the IL-15 expression of IL-15 by complementary DNA PCR. There was an inverse association between cell viability and CSE concentration, and NCI-H292 cells hardly survived at the CSE level more than 10% for 24-hour exposure. According to the cell viability, NCI-H292 cells were treated for 24 hours with the level of 5%, 2.5% and 1.25% CSE. Human NCI-H292 cells had the decreased IL-15 expression accompanied from the high to low CSE exposure, even more undetectable in 1.25% CSE treatment. Furthermore, in high dose and short-term CSE exposure, there was undetectable IL-15 expression after 10–50% CSE exposure for one hour, otherwise, we investigate NCI-H292 was back to express IL-15 at the third hour after 50% CSE exposure. These results suggest that CSE decreased NCI-H292 to express IL-15 expression regardless with high dose and short-term CSE exposure, or low dose and long-term CSE exposure. The lung epithelial carcinoma cells may defect the damage from cigarette smoke through IL-15 production. The Further study will demonstrate the mechanism of IL-15 expression in cytotoxicity.