Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer

Chiao-Hsiung Chuang, Hsiao Bai Yang, Shew Meei Sheu, Kuei Hsiang Hung, Jiunn Jong Wu, Hsiu-Chi Cheng, Wei-Lun Chang, Bor-Shyang Sheu

Research output: Contribution to journalArticle

19 Citations (Scopus)

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.

Original languageEnglish
Article number121
JournalBMC microbiology
Volume11
DOIs
Publication statusPublished - 2011 May 31

Fingerprint

Intestinal Neoplasms
Metaplasia
Helicobacter pylori
Stomach Neoplasms
Phosphorylation
Gastritis
Stomach
Coloring Agents
Stomach Ulcer
Duodenal Ulcer
Coculture Techniques
Tyrosine
Cell Culture Techniques
Odds Ratio
Biopsy
Infection
Proteins

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Microbiology (medical)

Cite this

@article{70af20016fa74c6ab2c004b0a5e4a11e,
title = "Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer",
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.",
author = "Chiao-Hsiung Chuang and Yang, {Hsiao Bai} and Sheu, {Shew Meei} and Hung, {Kuei Hsiang} and Wu, {Jiunn Jong} and Hsiu-Chi Cheng and Wei-Lun Chang and Bor-Shyang Sheu",
year = "2011",
month = "5",
day = "31",
doi = "10.1186/1471-2180-11-121",
language = "English",
volume = "11",
journal = "BMC Microbiology",
issn = "1471-2180",
publisher = "BioMed Central",

}

Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer. / Chuang, Chiao-Hsiung; Yang, Hsiao Bai; Sheu, Shew Meei; Hung, Kuei Hsiang; Wu, Jiunn Jong; Cheng, Hsiu-Chi; Chang, Wei-Lun; Sheu, Bor-Shyang.

In: BMC microbiology, Vol. 11, 121, 31.05.2011.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer

AU - Chuang, Chiao-Hsiung

AU - Yang, Hsiao Bai

AU - Sheu, Shew Meei

AU - Hung, Kuei Hsiang

AU - Wu, Jiunn Jong

AU - Cheng, Hsiu-Chi

AU - Chang, Wei-Lun

AU - Sheu, Bor-Shyang

PY - 2011/5/31

Y1 - 2011/5/31

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=79957508823&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79957508823&partnerID=8YFLogxK

U2 - 10.1186/1471-2180-11-121

DO - 10.1186/1471-2180-11-121

M3 - Article

C2 - 21619658

AN - SCOPUS:79957508823

VL - 11

JO - BMC Microbiology

JF - BMC Microbiology

SN - 1471-2180

M1 - 121

ER -