Document Type : Original Article
Authors
Department of Immunology, Medical School, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
Abstract
Background: Helicobacter pylori infection is one of the most common gastrointestinal infections worldwide. Predominant T-helper 1 (Th1) responses with increased gamma interferon (IFN- γ) levels have been proposed to play an important role in H. pylori-induced peptic ulcer. However, bacterial factors contributing to the initiation of Th1 polarization of H. pylori-specific immune responses have not been characterized.
Objective: Comparing serum concentrations of IL-18 in H. pylori-infected peptic ulcer (PU) patients, H. pylori-infected asymptomatic (AS) carriers and healthy control group and its association with bacterial virulence factor CagA.
Methods: Thirty H. pylori-infected PU patients (20 patients were positive for anti-CagA antibody and 10 patients were negative for anti-CagA antibody), 30 H. pylori-infected (AS) carriers (15 subjects with positive test for anti-CagA antibody and 15 subjects with negative test for anti-CagA antibody) and 20 healthy uninfected subjects were included in this study. Serum concentration of IL-18 was measured by ELISA method.
Results: The mean serum levels of IL-18 in PU patients (333.2 pg/ml ± 158), was significantly higher than those found in AS (146.5 pg/ml ± 90.1; P<0.001) and healthy control (82.2 pg/ml ± 45.7; P<0.0001). In both PU and AS groups, mean serum IL-18 levels in subjects with positive test for anti-CagA antibody were significantly higher than those observed in subjects with negative test for anti-CagA antibody. No significant difference was observed between serum IL-18 levels of healthy uninfected control and AS carriers with negative test for anti-CagA antibody.
Conclusion: The results of the present study showed higher serum concentrations of IL-18 in peptic ulcer patients compared with H.Pylori carriers and healthy controls. This difference in cytokine levels may be explained by differential expression of H.Pylori CagA gene during the course of the infection.
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