Role of Th22 cells in Helicobacter pylori-related gastritis and peptic ulcer diseases

Helicobacter pylori ( H. pylori ) has been shown to be one of the leading causes of peptic ulcer diseases (PUDs) and gastritis. T helper-22 (Th22) cells and its most important cytokine, interleukin-22 (IL-22) are importantly active in inflammation and inflammatory tissues. Since inflammation is one...

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Published in:Molecular biology reports Vol. 46; no. 6; pp. 5703 - 5712
Main Authors: Sanaii, Ahmad, Shirzad, Hedayatollah, Haghighian, Mehrnoosh, Rahimian, Ghorbanali, Soltani, Amin, Shafigh, Mohammadhadi, Tahmasbi, Kamran, Bagheri, Nader
Format: Journal Article
Language:English
Published: Dordrecht Springer Netherlands 01-12-2019
Springer Nature B.V
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Summary:Helicobacter pylori ( H. pylori ) has been shown to be one of the leading causes of peptic ulcer diseases (PUDs) and gastritis. T helper-22 (Th22) cells and its most important cytokine, interleukin-22 (IL-22) are importantly active in inflammation and inflammatory tissues. Since inflammation is one of the main attributes of infection caused by H. pylori and resulting complications (gastritis and gastrointestinal ulcer), this study was designed to evaluate the Th22 cells count and the IL-22 protein expression in people suffering from PUD and gastritis. The present study was conducted on 55 patients with gastritis, 47 patients with PUD and 48 uninfected subjects. After preparation of section and extraction of protein from antral biopsies, immunohistochemistry and western blot methods were used to evaluate the Th22 cells and IL-22 protein expression level, respectively. According to findings, the Th22 cells count and the IL-22 protein expression level in the infected subjects were siginficantly more than in the uninfected subjects. It should be noted that the Th22 cells count and the IL-22 protein expression level in the infected subjects with PUD were significantly greater than those in the infected subjects with gastritis. In addition, the Th22 cells count had positive correlation with the density of H. pylori , chronic inflammation score and acute inflammatory score in the infected subjects with PUD. The Th22 cells count had positive correlation with the Th17 cells count and inverse correlation with the Treg cells count in the infected subjects with PUD and gastritis. Our data demonstrated that abnormal hyper-activation of Th22 cells as well as its correlation with the Th17 cells during infection caused by H. pylori might damage tissues through immunopathological responses.
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ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-019-05004-1