Association of TNF-α but not IL-1β levels with the presence of Helicobacter pylori infection increased the risk of peptic ulcer development

摘要

Peptic ulcer is a lesion in the mucosa of the digestive tract affecting many people all around the world. Recent investigations have indicated that produced inflammatory cytokines such as TNF-α and IL-1β in response to gastric infection byHelicobacter pyloriplay an important role in the development of peptic ulcer. With regard to the significance of these cytokines in peptic ulcer development and the high prevalence of this disease in the developing countries, this study aimed to investigate the association of TNF-α and IL-1β with peptic ulcer in the presence ofH. pylori. This case-control study enrolled 61 patients with peptic ulcer disease (PUD) as cases and 59 people without peptic ulcer (NPUD) as controls. Blood samples and endoscopic biopsies were collected.H. pyloriinfection was confirmed by using rapid urease test (RUT), specific IgG measurement and histopathological examination. Then, IL-1β and TNF-α levels were evaluated using enzyme linked immunosorbent assay (ELISA). The seropositivity ofH. pyloriwas 62.5% in the studied population, while by considering RUT and histopathological examination along with specific-IgG antibody,H. pyloriinfection decreased to 56.7%. In addition,H. pyloriinfection was significantly (OR?=?0.37; 95% CI?=?0.17–0.82; P?=?.02) associated with peptic ulcer development. The TNF-α level in PUD and infectedH. pylorisubjects was significantly higher than that of control and un-infectedH. pyloriindividuals. However, no significant difference of IL1β level was observed between PUD and control groups as well as betweenH. pyloriinfected and un-infected individuals. Interestingly, IL-1β level in PUD patients withoutH. pyloriinfection was significantly higher than infected ones. Moreover, a significant correlation between specific-IgG antibody with TNF-α level was observed. Taken together, our results showed that increased level of TNF-α could probably play pivotal role in pathogenesis of peptic ulcer in the presence ofH. pyloriinfection. These findings also highlighted the importance of IL-1β in the absence ofH. pyloriinfection in peptic ulcer development.