Association between cag-pathogenicity island in Helicobacter pylori isolates from peptic ulcer, gastric carcinoma, and non-ulcer dyspepsia subjects with histological changes
Association between cag-pathogenicity island in Helicobacter pylori isolates from peptic ulcer, gastric carcinoma, and non-ulcer dyspepsia subjects with histological changes
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DOI:
10.3748/wjg.v11.i43.6815
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发表时间:
2005-11-21
影响因子:
4.3
通讯作者:
Habibullah, C. M.
中科院分区:
文献类型:
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作者:
Ali, Mahaboob;Khan, Aleem A.;Habibullah, C. M.
AIM: To investigate the presence of the cag-pathogenicity island and the associated histological damage caused by strains with complete cog-PAI and with partial deletions in correlation to the disease status.METHODS: We analyzed the complete cog-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 cog-PAL by polymerase chain reaction (PCR).RESULTS: The complete screening of the genes comprising the cog-PAL showed that larger proportions of subjects with gastric ulcer (97.8%) inhabited strains with complete cog-PAL, 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 cog-PAL were able to cause severe histological damage than with the partially deleted ones.CONCLUSION: The cog-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 cog-PAI appear to be sufficient to render the organism less pathogenic. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.