Lack of association among TNF-α gene expression, -308 polymorphism (G > A) and virulence markers of Helicobacter pylori.

Luanna Munhoz Zabaglia,Agostinho Caleman Neto,Mariane Avante Ferraz,Roger Willian De Labio,Marilia De Arruda Cardoso Smith,Spencer Luiz Marques Payão,Weendelly Nayara Pereira,Wilson Aparecido Orcini,Fernanda Wisnieski,Lucas Trevizani Rasmussen,Juliana Garcia De Oliveira

doi:10.1186/s40409-015-0054-3

Luanna Munhoz Zabaglia, Agostinho Caleman Neto + Show 9 more

Open Access

https://doi.org/10.1186/s40409-015-0054-3

Copy DOI

Abstract

BackgroundTumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients. Helicobacter pylori infection can induce a gastric mucosal inflammatory response that may be influenced by -308 (G > A) polymorphisms and gene expression of the TNF-α gene.MethodsOne hundred and thirty-four gastric biopsy samples were collected from patients of both genders (61♂ and 73♀, mean age 40.3 ± 24.2 years) with gastric symptoms. The -308 (G > A) polymorphism of TNF-α was characterized using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The expression level was measured using real-time PCR, and relative quantification (RQ) was calculated using the comparative CT method (2-ΔΔCT).ResultsThe analysis revealed an increase in TNF-α gene expression in patients with gastritis; on the other hand, no statistical differences were observed in patients with gastric cancer. In addition, no association was found among -308 polymorphism genotypes, virulence markers, or TNF-α gene expression.ConclusionsHelicobacter pylori induces a large increase in TNF-α expression in patients with gastritis, regardless of tissue inflammation, but after the tissue becomes neoplastic, the presence of bacteria did not influence expression. These results suggest that the TNF-α pathway may play an important role in the progression from gastritis to gastric cancer

Highlights

Tumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients
H. pylori presence was associated with the development of G and gastric cancer (GC) (p < 0.001), and an association between cagA and s1/m1 alleles of the vacuolating cytotoxin A (vacA) gene in samples from G and GC was observed (p < 0.001)
The group with gastric cancer tissue that tested negative for H. pylori was excluded due to the low sample number

Summary

Introduction

Tumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients. Helicobacter pylori (H. pylori) is a gram-negative bacterium that colonizes more than half of the world population, causing chronic infection. It comprises a major risk factor for gastric cancer (GC), which is the fourth most commonly diagnosed cancer and the second most deadly one, with over 750,000 new cases annually worldwide [1, 2]. Evidence suggests that the main pathophysiological event in the H. pylori infection of gastric mucosa is the induction of a gastric mucosal inflammatory response. This reaction is induced by the contact of H. pylori with gastric cells, and is followed by neutrophil and mononuclear cell activation and the transcription and synthesis of pro-inflammatory and anti-inflammatory cytokines [4, 5]

Objectives

Methods

Results

Conclusion