Douraghi Masoumeh, Mohammadi Marjan, Oghalaie Akbar, Abdirad Afshin, Mohagheghi Mohammad Ali, Hosseini Mahmoud Eshagh, Zeraati Hojat, Ghasemi Amir, Esmaieli Maryam, Mohajerani Nazanin
Department of Pathobiology, School of Public Health, Medical Sciences/University of Tehran, Tehran, Iran.
Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran, 13164.
J Med Microbiol. 2008 May;57(Pt 5):554-562. doi: 10.1099/jmm.0.47776-0.
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.
幽门螺杆菌十二指肠溃疡促进基因(dupA)先前已被描述为十二指肠溃疡(DU)发生的风险标志物以及胃癌(GC)的保护因子。最近评估dupA在临床结局预测中应用的研究存在争议。在本研究中,在伊朗患者中评估了dupA与幽门螺杆菌感染后的临床结局及组织病理学变化之间的关联。共评估了157例幽门螺杆菌感染患者,其中患有DU(n = 30)、胃溃疡(n = 23)、胃炎(n = 68)或GC(n = 36)。通过基因特异性PCR确定jhp0917和jhp0918基因的存在。根据更新的悉尼系统记录胃组织病理学变化。在157株检测菌株中,分别有78株(49.7%)和71株(45.2%)这两个基因呈阳性和阴性。157株菌株中其余8株(5.09%)为jhp0917阳性/jhp0918阴性。单因素分析显示dupA与组织学特征之间存在负相关,这些组织学特征包括作为GC倒数第二阶段的发育异常以及由于长期幽门螺杆菌相关性胃炎导致的淋巴滤泡。伊朗菌株与哥伦比亚、巴西和印度菌株的核苷酸序列同一性程度在jhp0917的比对区域为86.1%至100%,jhp0918为88%至98.8%,dupA基因部分序列为93.4%至99.5%。尽管在我们的人群中,如其他几个国家所报道的那样,拥有dupA基因与任何疾病类别均无关联,但幽门螺杆菌dupA阴性菌株与癌前病变的关联需要进一步研究以评估该基因作为GC保护标志物的作用。