Helicobacter pylori cagA Status and Peptic Ulcer Disease in Iran
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Helicobacterpylori contributes to the development of peptic ulcers and atrophic gastritis. Furthermore, H.pylori strains carrying the cagA gene are more virulent than cagA-negative strains and are associated with the development of gastric adenocarcinoma. The cagA gene is a putative H. pylori virulence factor of unknown function. The aim of this study was to determine the prevalence of the cagA gene among H. pylori isolates and its relationship with peptic ulcer disease in 128 Iranian patients. A total of 107 (83.6%) samples were positive, including 40 (95%) of the 42 patients with duodenal ulcer, 43 (86%) of the 50 patients with gastric ulcer, and 24 (66.6%) of the 36 patients with gastritis. cagA was present in 32 (80%) of 40 strains from duodenal ulcer patients, 33 (77%) of 43 strains from gastric ulcer patients, and 11 (46%) of 24 from gastritis patients. We also attempted to investigate the subtypes of 3′ region of cagA gene in H. pylori strains isolated from Iranian patients and their relation to H. pylori-associated gastroduodenal diseases. The PCR product of cagA positive strains obtained with primer set CAG1/CAG2 differed in size, varying from 642 to 651 bp (subtype A) in 33 isolates to 756 bp (subtype B/D) in 13 isolates. This does not support the view that subtypes of the 3′ region of cagA gene in H. pylori isolated from Iran correlate with the clinical outcomes of H. pylori, but colonization with cagA positive strains was significantly higher among duodenal ulcer than gastritis patients in Iran.
KeywordsHelicobacter pylori cagA Peptic ulcer
We would like to thank Zahra Shayegan for her helpful comments. This work was supported by University of Guilan.
- 8.Atherton JC, Cao P, Peek RM, Tummuru MKR, Blaser MJ, Cover TL (1995) Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J Biol Chem 270:17771–17777. doi: 10.1074/jbc.270.30.17771 PubMedCrossRefGoogle Scholar
- 16.Oliveira MJ, Costa AC, Costa AM, Henriques L, Suriano G, Atherton JC et al (2006) Helicobacter pylori induces gastric epithelial cell invasion in a c-Met and type IV secretion system-dependent manner. Biol Chem 46:34888–34896Google Scholar
- 20.Covacci A, Censini S, Bugnoli M, Petracca R, Burroni D, Macchia G et al (1993) Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci USA 90:5791–5795. doi: 10.1073/pnas.90.12.5791 PubMedCrossRefGoogle Scholar
- 22.Higashi H, Tsutsumi R, Fujita A, Yamazaki S, Asaka M, Azuma T et al (2002) Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites. Proc Natl Acad Sci USA 99:14428–14433. doi: 10.1073/pnas.222375399 PubMedCrossRefGoogle Scholar
- 36.Pan ZJ, van der Hulst RW, Feller M, Xiao SD, Tytgat GN, Dankert J et al (1997) Equally high prevalences of infection with cagA-positive Helicobacter pylori in Chinese patients with peptic ulcer disease and those with chronic gastritis-associated dyspepsia. J Clin Microbiol 35:1344–1347PubMedGoogle Scholar
- 38.Anderson H, Löivukene K, Sillakivi T, Maaroos HI, Ustav M, Peetsalu A et al (2002) Association of cagA and vacA genotypes of Helicobacter pylori with gastric diseases in Estonia. J Clin Microbiol 40:293–300Google Scholar