Wan Xiu-Kun, Yuan Sheng-Ling, Wang Yan-Chun, Tao Hao-Xia, Jiang Wei, Guan Zhang-Yan, Cao Cheng, Liu Chun-Jie
Xiu-Kun Wan, Sheng-Ling Yuan, Yan-Chun Wang, Hao-Xia Tao, Wei Jiang, Zhang-Yan Guan, Cheng Cao, Chun-Jie Liu, State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Biotechnology, Beijing 100071, China.
World J Gastroenterol. 2016 Dec 28;22(48):10566-10574. doi: 10.3748/wjg.v22.i48.10566.
To study the impact on cleavage of tumor necrosis factor receptor-associated factor 1 (TRAF1) regulated by ().
Cleavage of TRAF1 was detected by western blotting in the human gastric cancer cell line AGS following treatment with an apoptosis inducer. Cleavage of TRAF1 mediated by caspase was examined using specific caspase inhibitors. The effect of the COOH-terminal TRAF1 fragment on gastric cell apoptosis during infection was measured using flow cytometry. The impact of infection on TRAF1 cleavage was detected in the presence of apoptosis inducer. The roles of virulence factors that may regulate TRAF1 cleavage were analyzed using isogenic and null mutants.
TRAF1 was found to be cleaved in AGS cells treated with the apoptosis inducer, and caspase-8 was the major caspase involved in the cleavage of TRAF1. The COOH-terminal TRAF1 fragment significantly induced cell apoptosis ( < 0.05) as well as promoted -induced cell apoptosis ( < 0.05). infection was found to significantly inhibit the cleavage of TRAF1 and to inhibit the activation of caspase-8 in the presence of the apoptosis inducer at specific infection times and different cell/bacteria ratios. We also found that the effects of and null mutants on the inhibition of TRAF1 cleavage and activation of caspase-8 were significantly attenuated, compared with wild-type , in the presence of the apoptosis inducer, showing that the virulence factor CagA was mainly involved in the inhibition of TRAF1 cleavage.
infection significantly inhibits the cleavage of TRAF1 a CagA-dependent mechanism, which would increase the relative amounts of full-length TRAF1 and exert an antiapoptotic effect on -infected cells.
研究（）调控的肿瘤坏死因子受体相关因子1（TRAF1）裂解的影响。
用凋亡诱导剂处理人胃癌细胞系AGS后，通过蛋白质免疫印迹法检测TRAF1的裂解情况。使用特异性半胱天冬酶抑制剂检测半胱天冬酶介导的TRAF1裂解。采用流式细胞术检测感染期间TRAF1羧基末端片段对胃细胞凋亡的影响。在存在凋亡诱导剂的情况下检测感染对TRAF1裂解的影响。使用同基因和缺失突变体分析可能调控TRAF1裂解的毒力因子的作用。
发现用凋亡诱导剂处理的AGS细胞中TRAF1被裂解，且半胱天冬酶-8是参与TRAF1裂解的主要半胱天冬酶。TRAF1羧基末端片段显著诱导细胞凋亡（P<0.05），并促进幽门螺杆菌诱导的细胞凋亡（P<0.05）。发现在特定感染时间和不同细胞/细菌比例下，在存在凋亡诱导剂的情况下，幽门螺杆菌感染显著抑制TRAF1的裂解并抑制半胱天冬酶-8的激活。我们还发现，与野生型幽门螺杆菌相比，在存在凋亡诱导剂的情况下，突变体和缺失突变体对TRAF1裂解抑制和半胱天冬酶-8激活的作用显著减弱，表明毒力因子CagA主要参与TRAF1裂解的抑制。
幽门螺杆菌感染通过CagA依赖机制显著抑制TRAF1的裂解，这会增加全长TRAF1的相对量，并对幽门螺杆菌感染的细胞发挥抗凋亡作用。
需注意，原文中部分括号内容缺失，以上译文是在尽量完整理解文意基础上给出的。
