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

• Published in: BMC microbiology 2011-05, Vol.11 (1), p.121-121, Article 121
• Main Authors: Chuang, Chiao-Hsiung, Yang, Hsiao-Bai, Sheu, Shew-Meei, Hung, Kuei-Hsiang, Wu, Jiunn-Jong, Cheng, Hsiu-Chi, Chang, Wei-Lun, Sheu, Bor-Shyang
• Format: Article
• Language: English
• Subjects: Adult; Aged; Antigens, Bacterial - metabolism; Bacterial Proteins - metabolism; Biopsy; cagA; CagA phosphorylation; Care and treatment; Diagnosis; Dyspepsia; Female; gastric cancer; Gastric Mucosa - pathology; Genetic aspects; H. pylori; Health aspects; Helicobacter Infections - complications; Helicobacter Infections - pathology; Helicobacter pylori; Helicobacter pylori - metabolism; Helicobacter pylori - pathogenicity; Histocytochemistry; Humans; intestinal metaplasia; Male; Metaplasia - epidemiology; Metaplasia - etiology; Metaplasia - microbiology; Metaplasia - pathology; Middle Aged; Phosphorylation; Prospective Studies; Risk factors; Stomach cancer; Stomach Neoplasms - epidemiology; Stomach Neoplasms - etiology; Stomach Neoplasms - microbiology; Stomach Neoplasms - pathology
• ISSN: 1471-2180; 1471-2180
• DOI: 10.1186/1471-2180-11-121

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