【摘要】 目的探讨大肠埃希菌(E.coli)脂多糖(LPS)诱导树突状细胞(DCs)细胞系DC2.4吞噬并杀灭幽门螺杆菌(H.pylori)的可行性及其作用机制。方法将DC2.4分为对照组、E.coli LPS处理2h组和处理24h组;以流式细胞术(FCS)检测不同组DC2.4对H.pylori的吞噬量以及吞噬-溶酶体成熟标志蛋白溶酶体相关膜蛋白-1(LAMP-1)的表达量;以RT-qPCR检测相应组DC2.4中TLR4的表达。结果 DC2.4经E.coli LPS处理后对H.pylori的吞噬量明显增加(P=0.003),DC2.4吞噬H.pylori后吞噬-溶酶体成熟标志蛋白LAMP-1的表达量也明显增加(P=0.02);E.coli LPS处理的DC2.4吞噬H.pylori时TLR4的表达量增加(P=0.009)。结论 E.coli LPS可以诱导DCs对H.pylori的吞噬作用以及吞噬-溶酶体的成熟,有利于DCs对H.pylori的杀灭。E.coli LPS诱导杀灭作用的机制可能是解除了H.pylori对TLR4信号通路的抑制,为有效清除体内H.pylori感染提供了参考方向。更多还原

【Abstract】 Objective To study the effect and mechanism of E.coli lipopolysaccharide(LPS)on the phagocytosis of dendritic cells(DCs)to kill Helicobacter pylori.Methods DCs were divided into control group,2 h and 24 h LPS exposure groups.Flow cytometry was used to quantify the number of H.pylori inside the phagosome of DCs as well as the LAMP-1 amount.TLR4 expression was determined by RT-qPCR.Results Compared to the control group,exposure to LPS for 2 h and 24 h could significantly enhance the phagocytosic ablity of DCs to kill H.pylori(P<0.01),and the expression of LAMP-1 and TLR4 greatly increased(P<0.05,P<0.01).Conclusions The phagocytic ability of DCs can be enhanced by E.coli lipopolysaccharide to kill H.pylori.The possible mechanism is found that LPS may stimulate the downstream pathway of TLR4 in DCs which in turn helps to clear H.pylori infection in vivo.更多还原