Association Between Helicobacter pylori cagA, babA2 Virulence Factors and Gastric Mucosal Interleukin-33 mRNA Expression and Clinical Outcomes in Dyspeptic Patients

Shahi, Heshmat. and Reiisi, Somayeh. and Bahreini, Rasoul. and Bagheri, Nader. and Salimzadeh, Loghman. and shirzad, Hedayatollah. (2015) Association Between Helicobacter pylori cagA, babA2 Virulence Factors and Gastric Mucosal Interleukin-33 mRNA Expression and Clinical Outcomes in Dyspeptic Patients. INTERNATIONAL JOURNAL OF MOLECULAR AND CELLULAR MEDICINE, 4 (4). pp. 227-234.

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Abstract

Helicobacter pylori (H. pylori) infection has been reported in more than half of the world human population. It is associated with gastric inflammation and noticeable infiltration of the immune cells to the stomach mucosa by several cytokines secretion. IL-1 beta, IL-18 have been shown to contribute to H. pylori induced gastritis, but the details of inflammation and association of virulence factors remain unclear. IL-1 cytokine family has a new additional cytokine, Interleukin-33 (IL-33), which is contemplated to have an important role for host defense against microorganisms. H. pylori virulence factors important in gastritis risk are the cag pathogenicity island (cag-PAI) and babA. This study evaluated IL-33 mucosal mRNA expression levels in infected and uninfected patients and its relationship with bacterial virulence factors cagA, babA(2) and type of gastritis. Total RNA was extracted from gastric biopsies of 79 H. pylori-infected patients and 51 H. pylori-negative patients. Mucosal IL-33 mRNA expression levels in gastric biopsies were assessed using real-time PCR. Existence of virulence factors were detected by PCR. IL-33 mRNA expression was significantly higher in biopsies of H. pylori-infected patients compared to H. pylori-uninfected patients (P< 0.0001). Also there was a direct relationship between virulence factor bab-A2 and enhancement in IL-33 mRNA expression. Furthermore, IL-33 mRNA expression level was significantly lower in chronic gastritis patients compared with patients with active gastritis (P< 0.001). IL-33 may play a crucial role in the inflammatory response and induction of the chronic gastritis and severity of inflammatory changes in the gastric mucosa.

Item Type: Article
Uncontrolled Keywords: Helicobacter pylori; gastritis; interleukin-33; virulence factor
Subjects: WC Communicable Diseases
WI Digestive System
Divisions: Faculty of Medicine > Department of Clinical Sciences > Department of Internal Medicine
Reserach Vice-Chancellar Department > Cellular and Molecular Research Center
Depositing User: Users 1 not found.
Date Deposited: 19 Jul 2017 07:46
Last Modified: 20 May 2018 10:22
URI: http://eprints.skums.ac.ir/id/eprint/1590

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