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Altered Th17 Cytokine Expression in Helicobacter Pylori Patients With Tlr4 (D299g) Polymorphism Publisher Pubmed



Bagheri N1 ; Azadegandehkordi F2 ; Rahimian G3 ; Hashemzadehchaleshtori M2 ; Rafieiankopaei M4 ; Kheiri S5 ; Gholipour A2 ; Shirzad H2
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran
  3. 3. Department of Internal Medicine, Shahrekord University of Medical Sciences, Shahrekord, Iran
  4. 4. Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran
  5. 5. Biostatistics Department, Shahrekord University of Medical Sciences, Shahrekord, Iran

Source: Immunological Investigations Published:2016


Abstract

Helicobacter pylori (H. pylori) is associated with gastric ulcer and gastric adenocarcinoma. Polymorphisms in the host genes coding for Toll-like receptors (TLRs) may influence the innate and adaptive immune response to the infection, affecting the susceptibility to H. pylori or the disease outcomes. However, the details and association with different polymorphism and clinical expression of infection remain unclear. A case-control study consisting of 58 patients with H. pylori infection and 44 H. pylori uninfection was conducted. Genomic DNA was extracted and genotypes of TLR4 Asp299Gly polymorphism were assessed through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Mucosal cytokines expression in H. pylori-infected and uninfected gastric biopsies was determined by real-time PCR. The expression of IL-6, IL-17, IL-21, IL-23 and TGF-β1 was signicantly higher in patients with D299G polymorphism in TLR4. But the expression of IL-18 between patients with single-nucleotide polymorphisms (SNPs) in TLR4 and patients with the wild-type allele was not signicant. In H. pylori-infected patients with gastritis, SNPs in TLR4 may alter cytokine expression toward Th17 immune response in the gastric mucosa and may have increased risk for the development of peptic ulcer. © 2016 Taylor and Francis.