Role of the Helicobacter pylori-Induced inflammatory response in the development of gastric cancer

被引：259

作者：

Lamb, Acacia ^{[1
]}

Chen, Lin-Feng ^{[1
]}

机构：

[1] Univ Illinois, Coll Med, Dept Biochem, Urbana, IL USA

来源：

JOURNAL OF CELLULAR BIOCHEMISTRY | 2013年 / 114卷 / 03期

关键词：

Helicobacter pylori; INFLAMMATION; GASTRIC CANCER; NF-kappa B; NF-KAPPA-B; NEUTROPHIL-ACTIVATING PROTEIN; LYS63-LINKED POLYUBIQUITINATION; HP-NAP; CAGA; TAK1; EXPRESSION; SECRETION; CELLS; PHOSPHORYLATION;

D O I：

10.1002/jcb.24389

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：

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-?B in H. pylori-induced inflammation. J. Cell. Biochem. 114: 491497, 2013. (C) 2012 Wiley Periodicals, Inc.

引用

页码：491 / 497

页数：7

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