Transcriptional alteration in NF-κB-associated long noncoding RNAs in the gastric tissue of the Helicobacter pylori infected and non-infected patients with chronic gastritis

Abstract

Abstract Background: Helicobacter pylori could colonize the gastric mucosa and cause gastritis, gastric ulcer and gastric cancer. Numerous virulence factors have been identified in this bacterium that play important roles in the promotion of gastric disorders. Although the interaction of long noncoding RNAs (lncRNAs) with transcription, processing, and translation of genes associated with different diseases are described, their interaction with the inflammatory genes and H. pylori infection in the gastric tissue is not well known. In this study, H. pylori infection and its effect on the transcription of common lncRNAs that regulate NF-κB expression were analyzed relative to the non-infected patients. Materials and Methods: Two groups of H. pylori-infected and non-infected patients with chronic gastritis were included in the study after general histopathological and microbiological analysis. Genotyping of the H. pylori strains was done by PCR and relative changes in the expression of NF-κB and regulatory lncRNAs, lincRNA-p21, MALAT1, NKILA, were measured by relative quantitative real time-PCR. Results: Significant increase in the NF-κB gene expression was shown, while the expression level of MALAT1, lincRNA-p21 and NKILA genes decreased in the infected patients compared with the non-infected patients. Our results showed that the hypervirulent strain with oipA“on”/HP-NAP+/iceA1+/iceA2+/vacA s1m1/s1m2+/cagA+ genotype can promote a higher level of NF-κB transcription in the inflamed tissue. Conclusion: H. pylori infection could promote down-regulation of lincRNA-p21, MALAT1 and NKILA in the infected gastric tissue that is correlated with upregulation of NF-κB. More detailed studies are needed to show link between the virulence genes and their impact on the deregulation of lncRNAs in the gastric tissue.