Association between cag-pathogenicity island in Helicobacter pylori isolates from peptic ulcer,gastric carcinoma,and non-ulcer dyspepsia subjects with histological changes

AIM: To investigate the presence of the cay-pathogenicity island and the associated histological damage caused by strains with complete cay-PAI and with partial deletions in correlation to the disease status.METHODS: We analyzed the complete cag-PAI of 174representative Helicobacter pylori (H pylori ) clinical isolates obtained from patients with duodenal ulcer,gastric ulcer, gastric cancer, and non-ulcer dyspepsia using eight different oligonucleotide primers viz cagA1,cagA2, cagAP1, cagAP2, cagE, cagT, LEC-1, LEC-2spanning five different loci of the whole cag-PAI by polymerase chain reaction (PCR).RESULTS: The complete screening of the genes comprising the cag-PAI showed that larger proportions of subjects with gastric ulcer (97.8%) inhabited strains with complete cag-PAI, followed by gastric cancer (85.7%),non-ulcer dyspepsia (7.1%), and duodenal ulcer (6.9%),significant differences were found in the percentagedistribution of the genes in all the clinical groups studied.It was found that strains with complete cag-PAI were able to cause severe histological damage than with the partially deleted ones.CONCLUSION: The cay-PAI is a strong virulent marker in the disease pathogenesis as it is shown that a large number of those infected with strain with complete cag-PAI had one or the other of the irreversible gastric pathologies and interestingly 18.5% of them developed gastric carcinoma. The presence of an intact cayPAI correlates with the development of more severe pathology, and such strains were found more frequently in patients with severe gastroduodenal disease. Partial deletions of the cag-PAI appear to be sufficient to render the organism less pathogenic.

AIM： To investigate the presence of the cag-pathogenicity island and the associated histological damage caused by strains with complete cag-PAI and with partial deletions in correlation to the disease status. METHODS： We analyzed the complete cag-PAI of 174 representative Helicobacter pylori （H pylori ） clinical isolates obtained from patients with duodenal ulcer, gastric ulcer, gastric cancer, and non-ulcer dyspepsia using eight different oligonucleotide primers viz cagA1, cagA2, cagAP1, cagAP2, cagE, cagT, LEC-1, LEC-2 spanning five different loci of the whole cag-PAI by polymerase chain reaction （PCR）. RESULTS： The complete screening of the genes comprising the cag-PAI showed that larger proportions of subjects with gastric ulcer （97.8%） inhabited strains with complete cag-PAI, followed by gastric cancer （85.7%）, non-ulcer dyspepsia （7.1%）, and duodenal ulcer （6.9%）, significant differences were found in the percentage distribution of the genes in all the clinical groups studied. It was found that strains with complete cag-PAI were able to cause severe histological damage than with the partially deleted ones. CONCLUSION： The cag-PAI is a strong virulent marker in the disease pathogenesis as it is shown that a large number of those infected with strain with complete cag-PAI had one or the other of the irreversible gastric pathologies and interestingly 18.5% of them developed gastric carcinoma. The presence of an intact cag- PAI correlates with the development of more severe pathology, and such strains were found more frequently in patients with severe gastroduodenal disease. Partial deletions of the cag-PAI appear to be sufficient to render the organism less pathogenic.