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

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 dy...

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Autores principales: Chuang, Chiao-Hsiung, Yang, Hsiao-Bai, Sheu, Shew-Meei, Hung, Kuei-Hsiang, Wu, Jiunn-Jong, Cheng, Hsiu-Chi, Chang, Wei-Lun, Sheu, Bor-Shyang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117684/
https://www.ncbi.nlm.nih.gov/pubmed/21619658
http://dx.doi.org/10.1186/1471-2180-11-121
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author Chuang, Chiao-Hsiung
Yang, Hsiao-Bai
Sheu, Shew-Meei
Hung, Kuei-Hsiang
Wu, Jiunn-Jong
Cheng, Hsiu-Chi
Chang, Wei-Lun
Sheu, Bor-Shyang
author_facet Chuang, Chiao-Hsiung
Yang, Hsiao-Bai
Sheu, Shew-Meei
Hung, Kuei-Hsiang
Wu, Jiunn-Jong
Cheng, Hsiu-Chi
Chang, Wei-Lun
Sheu, Bor-Shyang
author_sort Chuang, Chiao-Hsiung
collection PubMed
description 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.
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spelling pubmed-31176842011-06-18 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 BMC Microbiol Research Article 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. BioMed Central 2011-05-27 /pmc/articles/PMC3117684/ /pubmed/21619658 http://dx.doi.org/10.1186/1471-2180-11-121 Text en Copyright ©2011 Chuang et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Chuang, Chiao-Hsiung
Yang, Hsiao-Bai
Sheu, Shew-Meei
Hung, Kuei-Hsiang
Wu, Jiunn-Jong
Cheng, Hsiu-Chi
Chang, Wei-Lun
Sheu, Bor-Shyang
Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
title Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
title_full Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
title_fullStr Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
title_full_unstemmed Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
title_short Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
title_sort helicobacter pylori with stronger intensity of caga phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117684/
https://www.ncbi.nlm.nih.gov/pubmed/21619658
http://dx.doi.org/10.1186/1471-2180-11-121
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