Effect of Helicobacter pylori on NFKB1, p38[alpha] and TNF-[alpha] mRNA expression levels in human gastric mucosa

• Published in: Experimental and therapeutic medicine 2016-06, Vol.11 (6), p.2365
• Main Authors: De Oliveira, Henrique Sulzbach, Biolchi, Vanderlei, Medeiros, Helouise Richardt, Jantsch, Daiane Bizerra Gandor, Delving, Luciana Knabben De Oliveira Becker, Reckziegel, Roberto, Goettert, Marcia Ines, Brum, Ilma Simoni, Pozzobon, Adriane
• Format: Article
• Language: English
• Subjects: Analysis; Gastric mucosa; Gene expression; Helicobacter pylori; Messenger RNA; Social class
• ISSN: 1792-0981
• DOI: 10.3892/etm.2016.3213

Helicobacter pylori infects ~50% of the world population, causing chronic gastritis and other forms of cellular damage. The present study assessed the influence of H. pylori on the mRNA expression levels of nuclear factor-[kappa]B1 (NFKB1), p38[alpha] and tumor necrosis factor-[alpha] (TNF-[alpha]) in human gastric mucosa in a southern Brazilian population. Human gastric tissue was collected by upper endoscopy and H. pylori diagnosis was performed using a rapid urease test and histological analysis. Total RNA was extracted and purified for subsequent cDNA synthesis and analysis by quantitative polymerase chain reaction (qPCR). The gastric tissue samples were divided into four groups as follows: Normal, inactive chronic gastritis, active chronic gastritis and intestinal metaplasia. The SDHA gene was classified as the most stable when compared with ACTB, GAPDH, B2M and HPRT1 genes, and was therefore selected as the reference gene for qPCR data normalization. TNF-[alpha] mRNA expression was significantly higher in samples that were positive for H. pylori and with active chronic gastritis. However, no difference was detected in the mRNA expression levels of NFKB1 and p38[alpha] between the groups. The present study concluded that the presence of H. pylori is associated with TNF-[alpha] upregulation in human gastric mucosa, but had no effect on NFKB1 and p38[alpha] mRNA expression levels. Key words: Helicobacter pylori, inflammation, gastritis, gene expression, quantitative polymerase chain reaction