Altered Cytokine Production in Patients with Helicobacter pylori Infection
Abdollah Safikhani Mahmoodzadeh1, Elham Moazamian1, Seyedeh Azra Shamsdin2
1Department of Microbiology, College of Sciences, Agriculture and Modern Technology, Shiraz Branch, Islamic Azad University, Shiraz, Iran.
Background:
Helicobacter pylori is a gram-negative pathogen. The infection caused by this pathogen may result in gastritis and can increase the risk of gastric cancer. This study investigated the relationship between H. pylori infection as the main risk factor for gastritis and changes in serum inflammatory cytokine levels.
Methods:
Blood samples from 85 patients with stomach pain, including 46 H. pylori-positive (Hp+) and 39 H. pylori-negative (Hp-) cases, were collected and referred to a gastroenterologist. After isolation and identification of H. pylori, the severity of gastritis was determined for each patient based on the histopathological findings. Finally, the serum levels of cytokines were measured using the multiplex kit and flow cytometry methods.
Results:
There were significant differences in the levels of interleukin-2 (IL-2), IL-4, IL-17A, IL-17F, IL-22, tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ) between the Hp- and the Hp+ specimens (P≤0.05). The levels of IL-2, IL-17A, IL-17F, IL-22, TNF-α, and IFN-γ were significantly higher in patients with mild and moderate gastritis than Hp- group (P≤0.05). In addition, IL-4 significantly increased in patients with moderate gastritis compared with Hp- individuals (P=0.008).
Conclusion:
Among the inflammatory cytokines evaluated in this study, IL-17A, IL-17F, and IL-22 may play a crucial role in developing moderate gastritis in infected patients with H. pylori.
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