Abstract
Cigarette smoke is related to many diseases. It causes cells oxidative damage and apoptosis, and affects the production of many cytokines. Interleukin 15 (IL-15) is a cytokine correlated with IL-2, and expressed mRNA constitutively in human airway epithelial cell. IL-15 receptor uses its own □ chain but shares the □ and □ chain with IL-2 receptor. IL-15 stimulates the proliferation, activation and recruitment of B cells, T cells and natural killer cells. IL-15 also transactivates the Axl receptor tyrosine kinase to protect fibroblast from apoptosis. This study was designed to investigate the responses of IL-15 as well as IL-2 against the inflammatory process induced by cigarette smoke extract (CSE) or lipopolysaccharide (LPS) in human airway epithelial cells. The gene expression were detected by reverse transcription polymerase chain reaction (PCR) and real-time PCR. The protein level in secrete form and cell surface investigated by enzyme-linked immunosorbent assay (ELISA) or flow cytometry. The results showed CSE prolonged the inflammation caused by LPS and induced the IL-15 and IL-2 mRNA expression independently. The presence of IL-15 protein was only detected on the cell membrane but not in the culture medium. This result suggested the signal transduction of IL-15 was through the way of transpresentation. The protein of IL-15R□ was increased when the concentration of CSE raised. And the mRNA of IL-15 and Axl was also induced by CSE. Increased Axl, IL-15 and IL-15R□ expression implied their synergistic role of resisting the CSE induced apoptosis. This study demonstrated the effect of CSE on the expression of IL-15 RNA and protein production during the inflammatory process. The IL-15 expression resisting CSE-induced apoptosis could be one of potential factors that CSE enhances the severity of airway diseases.