What a disorder: proinflammatory signaling pathways induced by Helicobacter pylori

被引:169
作者
Backert, Steffen [1 ]
Naumann, Michael [2 ]
机构
[1] Univ Coll Dublin, Sch Biomol & Biomed Sci, Dublin 4, Ireland
[2] Otto Von Guericke Univ, Inst Expt Internal Med, D-39120 Magdeburg, Germany
关键词
NF-KAPPA-B; GASTRIC EPITHELIAL-CELLS; CAG PATHOGENICITY ISLAND; TYROSINE PHOSPHORYLATION; IV SECRETION; ALPHA-PIX; HOST-CELL; C-MET; ACTIVATION; PROTEIN;
D O I
10.1016/j.tim.2010.08.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Infection of gastric epithelial cells with Helicobacter pylori induces strong proinflammatory responses by activating nuclear transcription factors NF-kappa B and AP-1. Several reports indicate that multiple bacterial factors and cellular molecules are involved in this signaling. Injected peptidoglycan, CagA or OipA and urease, and at least 16 different signaling cascades have been implicated in H. pylori-induced proinflammatory signaling. Many of these reports are contradictory, thus generating a highly puzzling scenario. Here we discuss the pros and cons of the multiple signaling activities in the induction of proinflammatory responses and associated problems, and give suggestions for finding ways out of this dilemma.
引用
收藏
页码:479 / 486
页数:8
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