Department of Biochemistry, College of Medicine, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
J Cell Biochem. 2013 Mar;114(3):491-7. doi: 10.1002/jcb.24389.
Helicobacter pylori (H. pylori) infection causes chronic gastritis and peptic ulceration and is the strongest risk factor for the development of gastric cancer. The pathogenesis of H. pylori is believed to be associated with infection-initiated chronic gastritis, which is characterized by enhanced expression of many inflammatory genes. H. pylori utilizes various virulence factors, targeting different cellular proteins, to modulate the host inflammatory response. In this review, we explore the many different ways by which H. pylori initiates inflammation, leveling many "hits" on the gastric mucosa which can lead to the development of cancer. We also discuss some recent findings in understanding the pathogen-host interactions and the role of transcription factor NF-κB in H. pylori-induced inflammation.
幽门螺杆菌（H. pylori）感染会导致慢性胃炎和消化性溃疡，并且是导致胃癌的最强风险因素。据信，H. pylori 的发病机制与感染引发的慢性胃炎有关，其特征是许多炎症基因的表达增强。H. pylori 利用各种毒力因子，靶向不同的细胞蛋白，来调节宿主的炎症反应。在这篇综述中，我们探讨了 H. pylori 引发炎症的许多不同方式，这些方式对胃黏膜造成了许多“打击”，从而导致癌症的发展。我们还讨论了一些最近在理解病原体-宿主相互作用以及转录因子 NF-κB 在 H. pylori 诱导的炎症中的作用方面的发现。
