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Zhang M.,Central Hospital OfHubei Xiangyang | Wang G.,Hubei University | Tao Y.,Chinese Institute of Aviation Medicine | Zhang H.,Chinese Institute of Aviation Medicine
Journal of B.U.ON. | Year: 2015

Purpose: To evaluate the proinflammatory effect and molecular mechanism of IL-17 in the intestinal epithelial cell line HT-29. Methods: After culture of HT-29 cells with IL-17 and/or TNF-α, real-time (RT) PCR and Western blot were used to measure the gene expression level of the neutrophil chemok- ines CXCL1, CXCL2, CXCL5, CXCL6, IL-8 and the Th-17 chemokine CCL20, the phosphorylation level of P38 and TNF-α, and the expression level of IL-8 after treatment with P38 inhibitor. Actl stable knockdown HT-29 cell line was established to further test the change of P38 phosphorylation after treatment with IL-17 and TNF-α. Results: When HT-29 cells were cultured with IL-17 and TNF-α, the expression level of neutrophil chemokines (CXCL1, CXCL2, CXCL5, CXCL6, IL-8) and Thl7 chemokine (CCL20) was significantly improved (24.96±2.53, 28.47±2.87,38.08±2.72,33A7±2A1, 31.7±2.38,44.37±2.73,respectively) (p<0.01). The results of Western blot showed that IL-17 obviously enhanced the phosphorylation of P38 induced by TNF-α. Compared with the control group, the expression level of IL-8 declined significantly (9.47±1.36 vs 3.06±0.67) when HT-29 was cultured together with IL-17 and TNF-α (p<0.01). P38 inhibition assay showed that P38 pathway played an essential role in IL-17 induced inflammatory response. The level of P38 phosphorylation could not be changed after treatment with IL-17 and TNF-α in Actl stable knockdown HT-29 cell line. Conclusion: IL-17 significantly promoted the gene expression level of TNF-α-induced neutrophil chemokines and Thl7 cells chemokine. IL-17 and TNF-α have an obvious synergistic effect on P38. Source

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