白介素 17 对脂多糖诱导人支气管上皮细胞炎症损伤的影响.

Objective: To investigate the effects of interleukin-17A (IL-17A) on lipopolysaccharide (LPS) -induced human bronchial epithelial cells (16-HBE) and their possible mechanisms. Methods: The 16-HBE cell line was cultured in vitro and intervened with LPS and IL-17A, and divided into blank control group, LPS group, IL-17A group and IL-17A+LPS group. The concentrations level of IL-4, IFN-γ, IL-6, IL-8 and other inflammatory factors in the supernatant of cell culture medium were determined by Enzyme linked immunosorbent assay(Elisa). The expression and activation of Mitogen-activated protein kinase(MAPKs) pathway related proteins: Phosphorylated extracellular regulated protein kinase (P-ERK), Extracellular regulated protein kinase (ERK), Phosphorylated P38 protein kinase (P-P38), P38 protein kinase (P38), Phosphorylated c-Jun N-terminal kinase (P-JNK), c-Jun N-terminal kinase (JNK) were detected byWestern Blotting (WB). The 16-HBE cell line was cultured in vitro and intervened with LPS, IL-17A, and ERK inhibitor(U0126), p38 inhibitor(SB203580), and JNK inhibitor (SP600125), and divided into blank control group, LPS + IL-17A group, IL-17A + LPS + UO126 group, IL-17A + LPS + SB203580 group, IL-17A + LPS + SP600125 group. Enzyme-linked immunosorbent assay was used to determine the levels of inflammatory factors such as IFN-γ, IL-4, IL-6, and IL-8 in the cell culture supernatant. Results: Compared with the blank control group, the concentration level of IL-6 and IL-8 were significantly increased in the cellular supernatant (P<0.01), while the concentration level of IL-4 was decreased (con vs LPS P<0.01, con vs IL-17A P<0.05) in the supernatant with either IL-17A or LPS stimulation. The expression of P-ERK, P-P38 and P-JNK protein was significantly increased (con vs LPS P<0.05, con vs IL-17A P<0.01). the concentration level of IL-6 and IL-8 were significantly increased (P<0.01). The levels of IL-6, IL-8, IL-4 and the expression of P-ERK, P-P38, and P-JNK in the cell supernatant of IL-17A + LPS group were higher than those in LPS and IL-17A group (P<0.05). After adding ERK, P38, and JNK inhibitors, compared with the LPS + IL-17A group, IL-17A + LPS + U0126 group, IL-17A + LPS + SB203580 group, and IL-17A + LPS + SP600125 group, the expression of IL-6, IL-8, IL-4 in cell supernatants has decreased (P<0.05). Conclusion: IL-17A might aggravate LPS-induced 16-HBE inflammatory injury by up-regulating IL-6 and IL-8 concentration level, and MAPKs may be an important signal transduction pathway in the process. [ABSTRACT FROM AUTHOR]