Proinflammatory effects and molecular mechanisms of interleukin-17 in intestinal epithelial cell line HT-29

作     者：Yi-Lin Wang Meng Fang Xiao-Ming Wang Wei-Yan Liu Yun-Jiang Zheng Xu-Bo Wu Ran Tao 

作者机构：Center for Organ Transplantation and Department of SurgeryRuijin HospitalShanghai Jiaotong University School of Medicine Department of General SurgeryMinhang HospitalFudan University Department of AnesthesiaThe 88th Hospital of PLA Department of Hepatobiliary SurgeryYijishan HospitalWannan Medical College Department of EmergencyXin Hua HospitalShanghai Jiaotong University School of Medicine 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2014年第20卷第47期

页      面：17924-17931页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：Supported by Minhang District Natural Science Foundation(to Wang YL) the Science and Technology Commission in Shanghai,No.10411968500 National Natural Science Foundation of China,No.81001324 

主　　题：IL-17 HT-29 TNF-α Inflammatory bowel disease 

摘      要：AIM:To evaluate the proinflammatory effects and molecular mechanisms of interleukin(IL)-17 in intestinal epithelial cell line ***:HT-29 cells were cultured with IL-17,tumor necrosis factor(TNF)-α,or the combination of both IL-17 and TNF-α.Real-time PCR and Western blot were used to measure the gene expression levels of neutrophil chemokines CXCL1,CXCL2,CXCL5,CXCL6,IL-8and TH-17 cell chemokine CCL20,the phosphorylation levels of p38 and TNF-α,and the expression level of IL-8,after using the p38 inhibitor in HT-29 *** stable Act1 knockdown HT-29 cell line was established to further test the phosphorylation changes of p38,after using IL-17 and TNF-α.RESULTS:After HT-29 cells were cultured with IL-17and TNF-α,the expression levels of neutrophil chemokines(CXCL1,CXCL2,CXCL5,CXCL6,IL-8)and Th17chemokine(CCL20)significantly improved(24.96±2.53,28.47±2.87,38.08±2.72,33.47±2.41,31.7±2.38,44.37±2.73,respectively),and the differences were all statistically significant(P0.01).Western blot results showed that IL-17 obviously enhanced the phosphorylation level of p38,which was induced by TNF-α.Compared with the control group,the expression level of IL-8 significantly declined(9.47±1.36 vs 3.06±0.67,P0.01)when TH-29 cells were cultured with IL-17and TNF-α.p38 inhibition assay showed that the p38pathway played an essential role in the inflammatory response induced by IL-17.p38 phosphorylation levels could not be changed after using IL-17 and TNF-αin the stable Act1 knockdown HT-29 cell ***:IL-17 significantly promoted the gene expression levels of TNF-α-induced neutrophil chemokines and Th17 cell *** is obvious that IL-17and TNF-αhave synergistic effects on p38.