Effect of Helicobacter pylori Eradication on TLR2 and TLR4 Expression in Patients with Gastric Lesions

Abstract

Objective. Helicobacter pylori (Hp) is recognized by TLR4 and TLR2 receptors, which trigger the activation of genes involved in the host immune response. Thus, we evaluated the effect of eradication therapy on TLR2 and TLR4 mRNA and protein expression in H. pylori-infected chronic gastritis patients (CG-Hp+) and 3 months after treatment. Methods. A total of 37 patients CG-Hp+ were evaluated. The relative quantification (RQ) of mRNA was assessed by TaqMan assay and protein expression by immunohistochemistry. Results. Before treatment both TLR2 and TLR4 mRNA in CG-Hp+ patients were slightly increased (TLR2 = 1.32; TLR4 = 1.26) in relation to Hp-negative normal gastric mucosa (P ≤ 0.05). After successful eradication therapy no significant change was observed (TLR2 = 1.47; TLR4 = 1.53; P > 0.05). In addition, the cagA and vacA bacterial genotypes did not influence the gene expression levels, and we observed a positive correlation between the RQ values of TLR2 and TLR4, both before and after treatment. Immunoexpression of the TLR2 and TLR4 proteins confirmed the gene expression results. Conclusion. In conclusion, the expression of both TLR2 and TLR4 is increased in CG-Hp+ patients regardless of cagA and vacA status and this expression pattern is not significantly changed after eradication of bacteria, at least for the short period of time evaluated.

Clinicopathological Features and Increased Expression of Toll-Like Receptor 4 of Gastric Cardia Cancer in a High-Risk Chinese Population

“…Previous studies suggested that TLR4 expression might be the link between H . pylori infection and cancer [ 31 , 37 , 58 ], and this expression pattern is not significantly changed after the eradication of bacteria [ 59 ]. In the present study, TLR4 expression was evaluated in a cohort of gastric cardia tissues.…”

Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection

“…Studies have shown that H. pylori infection deregulates host gene expression, such as receptors and co-receptors involved in bacterial recognition, signal transduction, immune and inflammatory response mediators, apoptosis, proliferation and metabolism-related genes in infected versus non-infected individuals (Hofman et al, 2007;Yang et al, 2012;Cadamuro et al, 2015). As a consequence, gene expression changes can influence the intensity of the host response against infection.…”

Host pathogen interactions in Helicobacter pylori related gastric cancer

“…Pathogen-associated molecular patterns (PAMPs) are various molecules of pathogenic microorganisms that in normal conditions are recognized by pattern recognition receptors (PRRs) resulting in triggering of the inflammatory response. H. pylori possess several mechanisms that prevent their recognition via Toll-like receptors (TLRs): (1) changing and rearranging LPS and flagellin; and (2) molecular mimicry between human Lewis and ABO blood group antigens and bacterial compounds, which confuses immune cells and prevents recognition of the pathogen[ 21 , 35 , 36 ]. It has been shown that the H. pylori flagellin is not detected by specific PRRs, and it does not stimulate the production of interleukin (IL)-8.…”