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Background: Diseases caused by Helicobacter pylori infection, including gastritis and gastric ulcer, can be harmful to epithelial cells in gastric mucosa. Furthermore, pro-inflammatory cytokines can affect the severity of some diseases caused by H. pylori infection. NLRP3 inflammasome detects H. pylori and activates caspase-1 that leads to the release of interleukin-1β (IL-1β) and interleukin-18 (IL-18) in the stomach. Objectives: Since genetic variations such as polymorphisms may be involved in the expression of genes, this study was conducted to investigate the effect of NLRP3 rs10754558 polymorphism in pathogenesis of H. pylori infection. Methods: Four hundred and sixty-four Iranian patients (300 patients infected with H. pylori and 164 patients uninfected with H. pylori) were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Cytokine mRNA and protein expression were evaluated in patients infected with different genotypes of NLRP3 rs10754558 using real time-PCR and western blotting, respectively. Results: The NLRP3 rs10754558 gene polymorphism was not associated with H. pylori infection or diseases caused by this bacterium. It was found out that the level of IL-1β in patients infected was higher than the uninfected individuals. Moreover, no relation was found between these single nucleotide polymorphisms and cytokine expression in H. pylori infected subjects. The findings of this study show that NLRP3 rs10754558 polymorphism may be related to the severity of acute inflammation in these patients. Conclusions: Our findings show that rs10754558 polymorphism might not participate in regulating inflammation and immune responses in patients with H. pylori by influencing the expression of components of the NLRP3 inflammasome.

Associations of a NLRP3 rs10754558 Polymorphism with Helicobacter pylori-Infected Patients with Gastritis and Peptic Ulcer Disease