» Articles » PMID: 21619658

Helicobacter Pylori with Stronger Intensity of CagA Phosphorylation Lead to an Increased Risk of Gastric Intestinal Metaplasia and Cancer

Overview
Journal BMC Microbiol
Publisher Biomed Central
Specialty Microbiology
Date 2011 May 31
PMID 21619658
Citations 10
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Nearly all Taiwanese H. pylori stains are cagA-genopositive and encode CagA protein. In this study, we evaluated whether different intensity of tyrosine phosphorylated-CagA (p-CagA) had an impact on the clinical diseases and histological outcomes in this area.

Results: We enrolled 469 dyspeptic patients and prospectively obtained the gastric biopsy specimens and the H. pylori isolates. These patients were categorized according to the clinical diseases, such as duodenal ulcer, gastric ulcer, gastric cancer, and gastritis with or without intestinal metaplasia. Their gastric specimens were reviewed by the updated Sydney's system. Furthermore, a total of 146 patients were randomly selected from each clinical category for evaluation of their isolates' p-CagA intensity by in vitro AGS cells co-culture. The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates. The isolates from the patients of gastric cancer or gastritis with intestinal metaplasia had stronger p-CagA intensity than those of gastritis without intestinal metaplasia (p ≤ 0.002). Moreover, the patients infected with isolates with strong or weak p-CagA intensity had a higher risk of gastric intestinal metaplasia (p < 0.05, odds ratio 3.09~15.26) than those infected with sparse p-CagA isolates.

Conclusions: Infection with H. pylori stains with stronger p-CagA intensity may lead to an increased risk of gastric intestinal metaplasia and cancer.

Citing Articles

The global prevalence of gastric cancer in Helicobacter pylori-infected individuals: a systematic review and meta-analysis.

Shirani M, Pakzad R, Haddadi M, Akrami S, Asadi A, Kazemian H BMC Infect Dis. 2023; 23(1):543.

PMID: 37598157 PMC: 10439572. DOI: 10.1186/s12879-023-08504-5.


HDAC6/FOXP3/HNF4α axis promotes bile acids induced gastric intestinal metaplasia.

Zhang L, Wang N, Chen M, Wu S, Zeng J, Zhou F Am J Cancer Res. 2022; 12(3):1409-1422.

PMID: 35411233 PMC: 8984877.


Bacterial CagA protein compromises tumor suppressor mechanisms in gastric epithelial cells.

Palrasu M, Zaika E, El-Rifai W, Garcia-Buitrago M, Piazuelo M, Wilson K J Clin Invest. 2020; 130(5):2422-2434.

PMID: 32250340 PMC: 7190987. DOI: 10.1172/JCI130015.


The impacts of H. pylori virulence factors on the development of gastroduodenal diseases.

Chang W, Yeh Y, Sheu B J Biomed Sci. 2018; 25(1):68.

PMID: 30205817 PMC: 6131906. DOI: 10.1186/s12929-018-0466-9.


Infection with CagA-positive Helicobacter pylori strain containing three EPIYA C phosphorylation sites is associated with more severe gastric lesions in experimentally infected Mongolian gerbils (Meriones unguiculatus).

Ferreira Junior M, Batista S, Vidigal P, Cordeiro A, Oliveira F, Prata L Eur J Histochem. 2015; 59(2):2489.

PMID: 26150158 PMC: 4503971. DOI: 10.4081/ejh.2015.2489.


References
1.
Polk D, Peek Jr R . Helicobacter pylori: gastric cancer and beyond. Nat Rev Cancer. 2010; 10(6):403-14. PMC: 2957472. DOI: 10.1038/nrc2857. View

2.
Yeh Y, Cheng H, Chang W, Yang H, Sheu B . Matrix metalloproteinase-3 promoter polymorphisms but not dupA-H. pylori correlate to duodenal ulcers in H. pylori-infected females. BMC Microbiol. 2010; 10:218. PMC: 2928200. DOI: 10.1186/1471-2180-10-218. View

3.
Batista S, Rocha G, Rocha A, Saraiva I, Cabral M, Oliveira R . Higher number of Helicobacter pylori CagA EPIYA C phosphorylation sites increases the risk of gastric cancer, but not duodenal ulcer. BMC Microbiol. 2011; 11:61. PMC: 3073878. DOI: 10.1186/1471-2180-11-61. View

4.
Atherton J, Blaser M . Coadaptation of Helicobacter pylori and humans: ancient history, modern implications. J Clin Invest. 2009; 119(9):2475-87. PMC: 2735910. DOI: 10.1172/JCI38605. View

5.
Wiedemann T, Loell E, Mueller S, Stoeckelhuber M, Stolte M, Haas R . Helicobacter pylori cag-Pathogenicity island-dependent early immunological response triggers later precancerous gastric changes in Mongolian gerbils. PLoS One. 2009; 4(3):e4754. PMC: 2650263. DOI: 10.1371/journal.pone.0004754. View