Helicobacter pylori flagellins have very low intrinsic activity to stimulate human gastric epithelial cells via TLR5
Helicobacter pylori flagellins have very low intrinsic activity to stimulate human gastric epithelial cells via TLR5
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DOI：
10.1016/j.micinf.2003.09.018
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发表时间：
2003-12-01
影响因子：
5.8
通讯作者：
Josenhans, C
中科院分区：
文献类型：
--
作者：
Lee, SK;Stack, A;Josenhans, C
幽门螺杆菌是一种鞭毛状的慢性病原体，它定植于胃粘液和粘膜细胞表面。鞭毛和运动是这种细菌在胃环境中生存所必需的。几种细菌的鞭毛蛋白通过与toll样受体5 （TLR5）结合而成为人类先天免疫系统的有效激活剂。本研究探讨了两种幽门螺杆菌鞭毛蛋白FlaA和FlaB在刺激人胃上皮细胞先天免疫系统和诱导IL-8释放中的可能作用。证实了TLR5在三种不同的人胃上皮细胞系中的转录和表达。大肠沙门氏菌血清型鼠伤寒沙门氏菌flc鞭毛蛋白能激活人胃上皮细胞。TLR5转录受幽门螺杆菌感染的调节。然而，这两种幽门螺杆菌鞭毛蛋白似乎没有通过TLR5对人胃细胞的免疫刺激潜力，尽管它们与其他细菌种类的鞭毛蛋白具有广泛的氨基酸同源性。这种独特的低激活电位鞭毛蛋白的进化发展被认为是幽门螺杆菌在胃的慢性定植过程中保持其鞭毛的基本功能和逃避有害宿主免疫反应的新机制。(C) 2003年版《科学与医学》Elsevier SAS。版权所有。
Helicobacter pylori is a flagellated chronic pathogen, which colonizes the gastric mucus and mucosal cell surfaces. Flagella and motility are essential for the survival of this bacterium in the stomach environment. Flagellins of several bacterial species are potent activators of the human innate immune system by binding to TOLL-like receptor 5 (TLR5). The possible role of the two H. pylori flagellins FlaA and FlaB in stimulation of the innate immune system and induction of IL-8 release by human gastric epithelial cells was investigated in this study. Transcription and expression of TLR5 in three different human gastric epithelial cell lines was demonstrated. Salmonella enterica serovar Typhimurium FliC flagellin was able to activate human gastric epithelial cells. TLR5 transcription was modulated by H. pylori infection. However, both H. pylori flagellins appeared to possess no immunostimulatory potential on human gastric cells via TLR5, despite their extensive amino acid homology to stimulating flagellins of other bacterial species. The evolutionary development of such unique flagellins of low activating potential is proposed to be a novel mechanism of H. pylori to preserve the essential function of its flagella during chronic colonization of the stomach and to evade the deleterious host immune responses. (C) 2003 Editions scientifiques et medicales Elsevier SAS. All rights reserved.