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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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Related in: MedlinePlus

Comparing with the isolates from patients without IM/cancer, those from cancer or IM patients had significantly stronger p-CagA intensity, more gastric atrophy, severer acute or chronic inflammation, but had no difference in H. pylori density. (The black, grey & white bars indicate: strong, weak, & spare p-CagA; dense, moderate & loose H. pylori density; severe, moderate & mild inflammation; with & without atrophy.)
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Figure 3: Comparing with the isolates from patients without IM/cancer, those from cancer or IM patients had significantly stronger p-CagA intensity, more gastric atrophy, severer acute or chronic inflammation, but had no difference in H. pylori density. (The black, grey & white bars indicate: strong, weak, & spare p-CagA; dense, moderate & loose H. pylori density; severe, moderate & mild inflammation; with & without atrophy.)

Mentions: In Figure 2, the H. pylori strains of gastric cancer or gastritis with IM patients had stronger p-CagA intensity than those of gastritis without IM (54.2% & 53.6% vs. 12.9%, p ≤ 0.002). There was also a trend that the H. pylori isolates from cancer or IM patients had relatively stronger p-CagA intensity then the subgroups of gastric and duodenal ulcer, but the difference was not significant. Moreover, the p-CagA intensity was not different among the subgroups of gastric ulcer, duodenal ulcer, and gastritis without IM. In Figure 3, the patients were separated according to having cancer risk or not. The isolates from the patients with cancer or IM had stronger p-CagA intensity than those from non-cancer/IM patients (p < 0.001). Furthermore, the patients with cancer risk had higher gastric inflammation or atrophy (p < 0.001).


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)

Comparing with the isolates from patients without IM/cancer, those from cancer or IM patients had significantly stronger p-CagA intensity, more gastric atrophy, severer acute or chronic inflammation, but had no difference in H. pylori density. (The black, grey & white bars indicate: strong, weak, & spare p-CagA; dense, moderate & loose H. pylori density; severe, moderate & mild inflammation; with & without atrophy.)
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Comparing with the isolates from patients without IM/cancer, those from cancer or IM patients had significantly stronger p-CagA intensity, more gastric atrophy, severer acute or chronic inflammation, but had no difference in H. pylori density. (The black, grey & white bars indicate: strong, weak, & spare p-CagA; dense, moderate & loose H. pylori density; severe, moderate & mild inflammation; with & without atrophy.)
Mentions: In Figure 2, the H. pylori strains of gastric cancer or gastritis with IM patients had stronger p-CagA intensity than those of gastritis without IM (54.2% & 53.6% vs. 12.9%, p ≤ 0.002). There was also a trend that the H. pylori isolates from cancer or IM patients had relatively stronger p-CagA intensity then the subgroups of gastric and duodenal ulcer, but the difference was not significant. Moreover, the p-CagA intensity was not different among the subgroups of gastric ulcer, duodenal ulcer, and gastritis without IM. In Figure 3, the patients were separated according to having cancer risk or not. The isolates from the patients with cancer or IM had stronger p-CagA intensity than those from non-cancer/IM patients (p < 0.001). Furthermore, the patients with cancer risk had higher gastric inflammation or atrophy (p < 0.001).

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