From genes polymorphisms to mucosal expression of cytokines: evaluating IL-23/IL-17 axis in adult patients with gastritis.

Fatemeh Azadegan-Dehkordi,Farid Zandi,Amin Talebi Bezmin Abadi,Razieh Sadat Hosseini,Parya Aslani,Ardeshir Abbasi,Khaled Minooie

doi:10.4314/ahs.v20i3.51

Abstract

Chronic inflammation is the typical sign of gastritis that may shift into gastric cancer. IL-17A and IL-17F as a novel inflammatory cytokines subset of CD4+Th play the main role in inflammation. A key cytokine receptor in the inflammatory IL-17/IL-23 axis, the interleukin 23 receptor (IL23R), may be related to gastritis. We evaluated the correspondence between IL-17A G197A, IL-17F A7488G and IL23R+2199 A/C polymorphisms with TGF-β1, IL-6, IL-17, IL-21 and IL-23 mucosal mRNAs expression in uninfected H. Pylori (HP) chronic gastritis patients. Total RNA and genomic DNA were separated from gastric biopsies of 44 patients with gastritis. Subsequently, mucosal mRNAs expression of TGF-β1, IL-6, IL-17, IL-21 and IL-23 were assessed by real-time PCR. To polymorphisms determination of IL-17A G197A, IL-17F A7488G and IL-23R +2199A/C the PCR-RFLP was used in gastric biopsies. Results point that IL-17A G197A, IL-17F A7488G and IL23R +2199A/C polymorphisms did not influence the mucosal expression of TGF-β1, IL-6, IL-17 and IL-21 (p> 0.05). In an opposite result, we don't find a correspondence between IL-17A G197A, IL-17F A7488G polymorphisms and mucosal expression of IL-23 (p> 0.05). In a contrary, we found a correlation between IL23R +2199A/C polymorphism and mucosal expression of IL-23 in patients with chronic gastritis (p< 0.05). These findings propose that IL23R +2199A/C polymorphism may change the mucosal expression of IL-23 pattern in patients with gastritis disease in the absence of HP, but to support the conclusion, more research may be required.

Highlights

There are a connection between inflammation in gastric mucosa, gastritis [1, 2] and infiltration immune cells, such as mononuclear and polynuclear cells, in the gastric mucosa that keeps up and expands the local in- AfricanHealth Sciences tribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.African Health Sciences Vol 20 Issue 3, September, 2020IL-23R play a significant role in the starting, keeping up and accelerating in the signaling of IL-23/IL-17 inflammatory axis 14
We have shown that IL-17A G197A, IL-17F A7488G and interleukin 23 receptor (IL23R) +2199A/C polymorphisms no alter the mucosal cytokine pattern in Iranian patients with H. Pylori (HP)-associated gastritis diseases31
We eliminate the role of HP as a side factor, it may lead to sharp result in our study, we suspect IL17A, IL-17F and IL23R genotypes confers an increased risk for development of gastritis and the rapid progression of gastric mucosal atrophy via affect the mucosal expression mRNA IL-17 and IL-23 in chronic gastritis stage

Summary

Introduction

There are a connection between inflammation in gastric mucosa, gastritis [1, 2] and infiltration immune cells, such as mononuclear and polynuclear cells, in the gastric mucosa that keeps up and expands the local in- AfricanHealth Sciences tribution License (https://creativecommons.org/licenses/BY/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.African Health Sciences Vol 20 Issue 3, September, 2020IL-23R play a significant role in the starting, keeping up and accelerating in the signaling of IL-23/IL-17 inflammatory axis 14. Our study suggests that these polymorphisms may alter the mucosal cytokine IL-23/IL-17 axis pattern by regulating TGF-β1, IL-6, IL-17, IL-21 and IL23 mucosal mRNAs produced and, probably, the consequent release of these cytokines. These changes can lead to development of severe histological changes in the gastric mucosa patients with gastritis without HP role (Fig.).

Methods

Results

Conclusion