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J Med Microbiol 57 (2008), 554-562; DOI: 10.1099/jmm.0.47776-0
© 2008 Society for General Microbiology
ISSN 1473-5644

dupA as a risk determinant in Helicobacter pylori infection

Masoumeh Douraghi1,2, Marjan Mohammadi1, Akbar Oghalaie1, Afshin Abdirad3, Mohammad Ali Mohagheghi3, Mahmoud Eshagh Hosseini4, Hojat Zeraati5, Amir Ghasemi2, Maryam Esmaieli1 and Nazanin Mohajerani1

1 Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran, 13164

2 Department of Pathobiology, School of Public Health, Medical Sciences/University of Tehran, Tehran, Iran

3 Cancer Research Center, Medical Sciences/University of Tehran, Tehran, Iran

4 Endoscopy Unit, Amiralam Hospital, Medical Sciences/University of Tehran, Tehran, Iran

5 Department of Biostatistics, School of Public Health, Medical Sciences/University of Tehran, Tehran, Iran

Correspondence
Marjan Mohammadi
marjan{at}pasteur.ac.ir
or
mmohammadi{at}yahoo.com

Received 20 November 2007
Accepted 6 January 2008

The Helicobacter pylori duodenal ulcer promoting (dupA) gene has been previously described as a risk marker for duodenal ulcer (DU) development and a protective factor against gastric cancer (GC). Recent studies which have assessed the application of dupA in the prediction of clinical outcomes have been controversial. In the current study, the association of dupA with the clinical outcomes and histopathological changes following H. pylori infection was evaluated in Iranian patients. A total of 157 H. pylori-infected patients with DU (n=30), gastric ulcer (n=23), gastritis (n=68) or GC (n=36) were assessed. The presence of jhp0917 and jhp0918 genes was determined by gene specific PCR. Gastric histopathological changes were recorded according to the updated Sydney system. Seventy-eight (49.7 %) and 71 (45.2 %) of the 157 tested strains, respectively, were positive and negative for both genes. The remaining 8 (5.09 %) of the 157 strains were jhp0917-positive/jhp0918-negative. Univariate analysis showed inverse associations between dupA and histological features including dysplasia as the penultimate stage of GC and lymphoid follicles as a consequence of relatively long-standing H. pylori-associated gastritis. The degrees of nucleotide sequence identity of Iranian strains to Colombian, Brazilian and Indian strains ranged from 86.1 to 100 % for the aligned regions of jhp0917, from 88 to 98.8 % for jhp0918 and from 93.4 to 99.5 % for the partial sequences of the dupA gene. Despite the fact that possession of the dupA gene showed no association with any disease category in our population as reported in several other countries, association of dupA-negative strains of H. pylori with pre-malignant lesions calls for additional studies to evaluate the role of this gene as a protective marker against GC.

Abbreviations: DU, duodenal ulcer; GC, gastric cancer; GU, gastric ulcer.

The GenBank/EMBL/DDBJ accession numbers for the target genes in this study are DQ865230, DQ865231, DQ865232, DQ865233, DQ865234, DQ865235, DQ865236, DQ865237, EF076755 and EF076756.




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Y. Yamaoka
Roles of the plasticity regions of Helicobacter pylori in gastroduodenal pathogenesis
J. Med. Microbiol., May 1, 2008; 57(5): 545 - 553.
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