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

Chuang CH, Yang HB, Sheu SM, Hung KH, Wu JJ, Cheng HC, Chang WL, Sheu BS - BMC Microbiol. (2011)

Bottom Line: 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.The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Internal Medicine, National Cheng Kung University, Tainan, Taiwan.

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.

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The H. pylori density, inflammation and atrophy by gastric histology among the 146 patients infected with H. pylori isolates with different p-CagA intensity. The isolates with stronger p-CagA intensity were significantly associated with more severe acute inflammation (p = 0.01) and chronic inflammation (p = 0.005) but not with H. pylori density or gastric atrophy (p = NS) (Pearson chi-square test).
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Figure 4: The H. pylori density, inflammation and atrophy by gastric histology among the 146 patients infected with H. pylori isolates with different p-CagA intensity. The isolates with stronger p-CagA intensity were significantly associated with more severe acute inflammation (p = 0.01) and chronic inflammation (p = 0.005) but not with H. pylori density or gastric atrophy (p = NS) (Pearson chi-square test).

Mentions: In Figure 4, this study also analyzed whether there were an association between the p-CagA intensity and the severity of gastric inflammation in histology. The patients infected with H. pylori isolates with stronger p-CagA intensity may have more severe acute inflammation (p = 0.04) and also chronic inflammation (p = 0.002). Nevertheless, the p-CagA intensity of H. pylori isolates was not associated with the HPD or gastric atrophy (p > 0.05).


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

Chuang CH, Yang HB, Sheu SM, Hung KH, Wu JJ, Cheng HC, Chang WL, Sheu BS - BMC Microbiol. (2011)

The H. pylori density, inflammation and atrophy by gastric histology among the 146 patients infected with H. pylori isolates with different p-CagA intensity. The isolates with stronger p-CagA intensity were significantly associated with more severe acute inflammation (p = 0.01) and chronic inflammation (p = 0.005) but not with H. pylori density or gastric atrophy (p = NS) (Pearson chi-square test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3117684&req=5

Figure 4: The H. pylori density, inflammation and atrophy by gastric histology among the 146 patients infected with H. pylori isolates with different p-CagA intensity. The isolates with stronger p-CagA intensity were significantly associated with more severe acute inflammation (p = 0.01) and chronic inflammation (p = 0.005) but not with H. pylori density or gastric atrophy (p = NS) (Pearson chi-square test).
Mentions: In Figure 4, this study also analyzed whether there were an association between the p-CagA intensity and the severity of gastric inflammation in histology. The patients infected with H. pylori isolates with stronger p-CagA intensity may have more severe acute inflammation (p = 0.04) and also chronic inflammation (p = 0.002). Nevertheless, the p-CagA intensity of H. pylori isolates was not associated with the HPD or gastric atrophy (p > 0.05).

Bottom Line: 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.The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Internal Medicine, National Cheng Kung University, Tainan, Taiwan.

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.

Show MeSH
Related in: MedlinePlus