OBJECTIVE: Helicobacter pylori is an important factor in the development of duodenal ulcer disease and has been implicated in the pathogenesis of gastric adenocarcinoma. It has been suggested that the cagA gene is a marker for more virulent strains of H. pylori. METHODS: We determined the prevalence of the cagA gene in 60 clinical isolates [34 from gastric carcinoma patients (CA), 26 from duodenal ulcer patients (DU)] from Korea, a country with a high incidence and mortality from gastric cancer. Genomic DNA was polymerase chain reaction-amplified by using two different primer sets for the cagA gene. The first cagA primer set amplifies a 297-bp product from the midregion of the cagA gene. The second primer set, which was previously established in a patient population from the Houston area (21 DU patients, 20 from individuals with asymptomatic gastritis) amplified a 1.4-kb region further downstream in the cagA gene. RESULTS: The expected 297 bp polymerase chain reaction amplicon for cagA was identified in 59/60 (98.3%) H. pylori isolates from Korea (33/34 CA, 26/26 DU), and in 36/41 (88%) isolates from the Houston area (20/21 DU, 16/20 asymptomatic gastritis) (NS). Using the second cagA primer set, the expected 1.4-kb product was found in only 1/60 (1.7%) H. pylori isolates from Korea (1/34 CA, 0/26 DU), and in 36/41 (88%) of isolates from the Houston area (20/21 DU, 16/20 GST) (p < 0.001). Western blot analysis showed that all Korean H. pylori isolates expressed cagA. CONCLUSIONS: The high prevalence of the cagA gene in H. pylori isolates from Korean patients with gastric adenocarcinoma or duodenal ulcers indicates that the cagA gene is common in H. pylori strains, and therefore, is not reliable as a single marker for the discrimination of H. pylori strains with respect to a specific disease. Our data further suggest that allelic variations in the genome of H. pylori strains may exist and that distinct H. pylori populations may circulate in different geographic regions.
OBJECTIVE:Helicobacter pylori is an important factor in the development of duodenal ulcer disease and has been implicated in the pathogenesis of gastric adenocarcinoma. It has been suggested that the cagA gene is a marker for more virulent strains of H. pylori. METHODS: We determined the prevalence of the cagA gene in 60 clinical isolates [34 from gastric carcinomapatients (CA), 26 from duodenal ulcerpatients (DU)] from Korea, a country with a high incidence and mortality from gastric cancer. Genomic DNA was polymerase chain reaction-amplified by using two different primer sets for the cagA gene. The first cagA primer set amplifies a 297-bp product from the midregion of the cagA gene. The second primer set, which was previously established in a patient population from the Houston area (21 DU patients, 20 from individuals with asymptomatic gastritis) amplified a 1.4-kb region further downstream in the cagA gene. RESULTS: The expected 297 bp polymerase chain reaction amplicon for cagA was identified in 59/60 (98.3%) H. pylori isolates from Korea (33/34 CA, 26/26 DU), and in 36/41 (88%) isolates from the Houston area (20/21 DU, 16/20 asymptomatic gastritis) (NS). Using the second cagA primer set, the expected 1.4-kb product was found in only 1/60 (1.7%) H. pylori isolates from Korea (1/34 CA, 0/26 DU), and in 36/41 (88%) of isolates from the Houston area (20/21 DU, 16/20 GST) (p < 0.001). Western blot analysis showed that all Korean H. pylori isolates expressed cagA. CONCLUSIONS: The high prevalence of the cagA gene in H. pylori isolates from Korean patients with gastric adenocarcinoma or duodenal ulcers indicates that the cagA gene is common in H. pylori strains, and therefore, is not reliable as a single marker for the discrimination of H. pylori strains with respect to a specific disease. Our data further suggest that allelic variations in the genome of H. pylori strains may exist and that distinct H. pylori populations may circulate in different geographic regions.
Authors: E K Ng; S A Thompson; G I Pérez-Pérez; I Kansau; A van der Ende; A Labigne; J J Sung; S C Chung; M J Blaser Journal: Clin Diagn Lab Immunol Date: 1999-05
Authors: A A Ashour; G B Collares; E N Mendes; V R de Gusmão; D M Queiroz; P P Magalhães; A S de Carvalho; C A de Oliveira; A M Nogueira; G A Rocha; A M Rocha Journal: J Clin Microbiol Date: 2001-05 Impact factor: 5.948
Authors: Karen Miernyk; Julie Morris; Dana Bruden; Brian McMahon; Debby Hurlburt; Frank Sacco; Alan Parkinson; Thomas Hennessy; Michael Bruce Journal: J Clin Microbiol Date: 2011-07-13 Impact factor: 5.948
Authors: S Miehlke; A Meining; A Morgner; E Bayerdörffer; N Lehn; M Stolte; D Y Graham; M F Go Journal: J Clin Microbiol Date: 1998-08 Impact factor: 5.948
Authors: C Pagliaccia; M de Bernard; P Lupetti; X Ji; D Burroni; T L Cover; E Papini; R Rappuoli; J L Telford; J M Reyrat Journal: Proc Natl Acad Sci U S A Date: 1998-08-18 Impact factor: 11.205
Authors: L J van Doorn; C Figueiredo; R Sanna; S Pena; P Midolo; E K Ng; J C Atherton; M J Blaser; W G Quint Journal: J Clin Microbiol Date: 1998-09 Impact factor: 5.948