University College Dublin, School of Biomolecular and Biomedical Sciences, Belfield Campus, Dublin 4, Ireland.
Trends Microbiol. 2010 Nov;18(11):479-86. doi: 10.1016/j.tim.2010.08.003. Epub 2010 Sep 20.
Infection of gastric epithelial cells with Helicobacter pylori induces strong proinflammatory responses by activating nuclear transcription factors NF-κB 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.
幽门螺杆菌感染胃上皮细胞可通过激活核转录因子 NF-κB 和 AP-1 诱导强烈的促炎反应。有几项报道表明,多种细菌因子和细胞分子参与了这一信号转导。已发现注入的肽聚糖、CagA 或 OipA 和脲酶以及至少 16 种不同的信号级联反应与 H. pylori 诱导的促炎信号转导有关。其中许多报道相互矛盾,因此产生了一个非常令人困惑的情况。在这里,我们讨论了在诱导促炎反应和相关问题中多种信号活性的优缺点,并为如何解决这一困境提出了建议。