AIM: To establish stock of clinical Helicobacter pylori (H. pylori) isolates, to perform cagA and vacA typing of these isolates, to evaluate the relationship between genotypes of cagA and vacA and upper gastrointestinal diseases and to assess the association of vacA genotypes with presence of the pathogenicity marker-cagA. METHODS: Clinical H.pylori strains were isolated from the antrum of 259 patients in Clumbia agar. The isolated H.pylori strains were identified by histology, and16SrRNA PCR. CagA genotypes were detected by colony hybridization, the probe was derived from the cloned plasmid PcagA, and digested by EcoRI-HindIII and the isolated PcagA DNA fragment was radioactively labelled by the random priming method. vacA genes types (s,m)and subtypes (s1a, s1b, s2) were typed by PCR. Vacuolating toxin was detected with neutral red absorb test. The results were treated statistically by chi(2) test, t test, and rank sum test. RESULTS: A total of 192 clinical H.pylori strains were isolated and the stock of Helicobacter pylori was established. The total positive rate of cagA was 87 % in all gastric diseases, and 95 % in gastric cancer group. There was a difference between gastric cancer group and the other groups (P<0.05) except duodenal ulcer group. The expression of type s1 of vacA was more than type s2 (P<0.05), and, the expression of type m1 was equal to type m2. In gastric cancer group, there was a difference between s1a and s1b (P<0.05), and s1a was more than s1b. Vacuolating toxins were more in Xi'an area isolates. CONCLUSION: The cagA(+) vacA type s1 clinical isolates are more in Xi'an area, but this can not serve as an index to predict gastric cancer.
AIM: To establish stock of clinical Helicobacter pylori (H. pylori) isolates, to perform cagA and vacA typing of these isolates, to evaluate the relationship between genotypes of cagA and vacA and upper gastrointestinal diseases and to assess the association of vacA genotypes with presence of the pathogenicity marker-cagA. METHODS: Clinical H.pylori strains were isolated from the antrum of 259 patients in Clumbia agar. The isolated H.pylori strains were identified by histology, and16SrRNA PCR. CagA genotypes were detected by colony hybridization, the probe was derived from the cloned plasmid PcagA, and digested by EcoRI-HindIII and the isolated PcagA DNA fragment was radioactively labelled by the random priming method. vacA genes types (s,m)and subtypes (s1a, s1b, s2) were typed by PCR. Vacuolating toxin was detected with neutral red absorb test. The results were treated statistically by chi(2) test, t test, and rank sum test. RESULTS: A total of 192 clinical H.pylori strains were isolated and the stock of Helicobacter pylori was established. The total positive rate of cagA was 87 % in all gastric diseases, and 95 % in gastric cancer group. There was a difference between gastric cancer group and the other groups (P<0.05) except duodenal ulcer group. The expression of type s1 of vacA was more than type s2 (P<0.05), and, the expression of type m1 was equal to type m2. In gastric cancer group, there was a difference between s1a and s1b (P<0.05), and s1a was more than s1b. Vacuolating toxins were more in Xi'an area isolates. CONCLUSION: The cagA(+) vacA type s1 clinical isolates are more in Xi'an area, but this can not serve as an index to predict gastric cancer.
Authors: C A Fallone; A N Barkun; M U Göttke; L M Best; V G Loo; S Veldhuyzen van Zanten; T Nguyen; A Lowe; T Fainsilber; K Kouri; R Beech Journal: Am J Gastroenterol Date: 2000-03 Impact factor: 10.864
Authors: Diana M Cittelly; Mónica G Huertas; Julián D Martínez; Ricardo Oliveros; Héctor Posso; María Mercedes Bravo; Oscar Orozco Journal: Rev Med Chil Date: 2002-02 Impact factor: 0.553