Miftahussurur Muhammad, Yamaoka Yoshio
a 1 Oita University, Airlangga University, Surabaya, Indonesia.
b 2 Oita University, Baylor College of Medicine, Houston, USA.
Expert Rev Gastroenterol Hepatol. 2015;9(12):1535-47. doi: 10.1586/17474124.2015.1095089. Epub 2015 Oct 16.
Helicobacter pylori infection plays an important role in the pathogenesis of peptic ulcer disease (PUD). Several factors have been proposed as possible H. pylori virulence determinants; for example, bacterial adhesins and gastric inflammation factors are associated with an increased risk of PUD. However, differences in bacterial virulence factors alone cannot explain the opposite ends of the PUD disease spectrum, that is duodenal and gastric ulcers; presumably, both bacterial and host factors contribute to the differential response. Carriers of the high-producer alleles of the pro-inflammatory cytokines IL-1B, IL-6, IL-8, IL-10, and TNF-α who also carry low-producer allele of anti-inflammatory cytokines have severe gastric mucosal inflammation, whereas carriers of the alternative alleles have mild inflammation. Recent reports have suggested that the PSCA and CYP2C19 ultra-rapid metabolizer genotypes are also associated with PUD.
幽门螺杆菌感染在消化性溃疡病（PUD）的发病机制中起重要作用。已经提出了几种因素作为幽门螺杆菌可能的毒力决定因素；例如，细菌黏附素和胃炎症因子与PUD风险增加有关。然而，仅细菌毒力因子的差异无法解释PUD疾病谱的两端，即十二指肠溃疡和胃溃疡；据推测，细菌和宿主因素都导致了这种不同的反应。促炎细胞因子IL-1B、IL-6、IL-8、IL-10和TNF-α的高产等位基因携带者，同时携带抗炎细胞因子低产等位基因，会出现严重的胃黏膜炎症，而携带其他等位基因的携带者炎症较轻。最近的报告表明，PSCA和CYP2C19超快代谢基因型也与PUD有关。
