The Helicobacter pylori cag pathogenicity island as a determinant of gastric cancer risk

被引:29
作者
Tran, Sirena C. [1 ]
Bryant, Kaeli N. [1 ]
Cover, Timothy L. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Vanderbilt Univ, Dept Pathol Microbiol & Immunol, Med Ctr, Nashville, TN USA
[2] Vanderbilt Univ, Dept Med, Sch Med, Nashville, TN USA
[3] Vanderbilt Univ, Vanderbilt Inst Infect Immunol & Inflammat, Med Ctr, Nashville, TN USA
[4] Vet Affairs Tennessee Valley Healthcare Syst, Nashville, TN USA
[5] Vanderbilt Univ, Med Ctr North A2200, Sch Med, Div Infect Dis,Dept Med, Nashville, TN 37232 USA
基金
美国国家卫生研究院;
关键词
Helicobacter pylori; gastric cancer; inflammation; bacterial secretion system; effector protein; VIRULENCE FACTOR CAGA; IV SECRETION; TYROSINE PHOSPHORYLATION; TUMOR-SUPPRESSOR; DUODENAL-ULCER; BIOLOGICAL-ACTIVITY; CLINICAL-RELEVANCE; EPITHELIAL-CELLS; VACA GENOTYPES; BETA-CATENIN;
D O I
10.1080/19490976.2024.2314201
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Helicobacter pylori strains can be broadly classified into two groups based on whether they contain or lack a chromosomal region known as the cag pathogenicity island (cag PAI). Colonization of the human stomach with cag PAI-positive strains is associated with an increased risk of gastric cancer and peptic ulcer disease, compared to colonization with cag PAI-negative strains. The cag PAI encodes a secreted effector protein (CagA) and components of a type IV secretion system (Cag T4SS) that delivers CagA and non-protein substrates into host cells. Animal model experiments indicate that CagA and the Cag T4SS stimulate a gastric mucosal inflammatory response and contribute to the development of gastric cancer. In this review, we discuss recent studies defining structural and functional features of CagA and the Cag T4SS and mechanisms by which H. pylori strains containing the cag PAI promote the development of gastric cancer and peptic ulcer disease.
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