dupA as a risk determinant in Helicobacter pylori infection.
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.
Douraghi
Masoumeh
M
Department of Pathobiology, School of Public Health, Medical Sciences/University of Tehran, Tehran, Iran.|Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran, 13164.
Mohammadi
Marjan
M
Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran, 13164.
Oghalaie
Akbar
A
Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran, 13164.
Abdirad
Afshin
A
Cancer Research Center, Medical Sciences/University of Tehran, Tehran, Iran.
Mohagheghi
Mohammad Ali
MA
Cancer Research Center, Medical Sciences/University of Tehran, Tehran, Iran.
Hosseini
Mahmoud Eshagh
ME
Endoscopy Unit, Amiralam Hospital, Medical Sciences/University of Tehran, Tehran, Iran.
Zeraati
Hojat
H
Department of Biostatistics, School of Public Health, Medical Sciences/University of Tehran, Tehran, Iran.
Ghasemi
Amir
A
Department of Pathobiology, School of Public Health, Medical Sciences/University of Tehran, Tehran, Iran.
Esmaieli
Maryam
M
Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran, 13164.
Mohajerani
Nazanin
N
Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran, 13164.
D001483:Base Sequence; D004381:Duodenal Ulcer / Q000382:microbiology; D041981:Gastrointestinal Tract / Q000382:microbiology / Q000473:pathology; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology; D005819:Genetic Markers; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics / Q000378:metabolism* / Q000472:pathogenicity; D006801:Humans; D007492:Iran; D008969:Molecular Sequence Data; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000382:microbiology; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics / Q000378:metabolism*
C528428:DupA protein, Helicobacter pylori; D005819:Genetic Markers; D037521:Virulence Factors