Abstract
Background/Aim: A considerable high number of dyspeptic patients were reported even with the decreasing prevalence of <i>H. pylori </i>in Sri Lanka. Several microbial, host, and environmental factors may associate with the disease outcome. Pyrin secreted by the white blood cells may modulate the inflammatory process by assembling inflammasome complexes in response to pathogen infection. This study focused on the role of pyrin gene polymorphism in gastric mucosal severity and <i>H. pylori</i> infection. Materials and Methods: Among the ninety dyspeptic patients three gastric biopsies were taken and the presence of <i>H. pylori</i>, yeast species and the gastric mucosal severity was determined. EDTA blood was used for DNA extraction and identification of pyrin gene polymorphism. 12 MEFV gene mutations were tested. Results: Most of the patients (61%) had mild chronic gastritis. Among them 11.1% specimens gave positive bands for NL1/LS2 PCR of yeast DNA. <i>H. pylori</i> was positive in 17 patients. No homozygous mutations were found in the MEFV gene. The most common three heterozygous mutations were E148Q (45%), P369S (5%), M680I (11.6%). No significant difference was observed between the presence of the gene polymorphism, gastric mucosal severity or the presence of <i>H. pylori</i> and yeast species in the study group. Conclusion: The absence of homozygous mutations in the MEFV gene suggests that it is not a main factor contributing to gastric mucosal severity. The presence of <i>H. pylori</i> and yeasts reinforce the concept that stomach is a non-sterile environment.
Highlights
The human stomach is considered a sterile organ
There has been a Yashodha Weerasinghe et al.: Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study decreasing incidence of H. pylori in recent years reported in Sri Lanka [5]
Study demonstrated the presence of heterozygous mutations in E148Q, P369S, M6801 and absence of homozygous mutations in the study population
Summary
The human stomach is considered a sterile organ. The unfavorable environment for microbial colonization is due to the inherent acidic environment, thick mucus layer, and gastric peristalsis [1]. Recent studies have focused on the host immune-regulatory response against the gastric mucosal inflammation caused by H. pylori. There has been no considerable decline in patients seeking treatment for dyspepsia Endoscopic investigations of these patients often reveal inflammatory changes in their gastric mucosa with varying severity despite the low H. pylori prevalence [6]. It is important to investigate other possible microbial etiologies contributing to gastric inflammation. Among the host genetic factors that could influence the gastric microbiota and inflammation are pyrin and pro-inflammatory cytokines [7]. Pyrin in the gastric mucosa modulates the inflammatory process by, assembling inflammasome complexes in response to pathogen infection [8]. Pyrin may have a role in modulation of the inflammatory response resulting in the alteration of the microbial flora together which may contribute to gastric pathology
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
