Potential role of human β-defensin 1 in Helicobacter pylori-induced gastritis

Objective. Helicobacter pylori-induced gastric inflammation is dependent on the persistence of the microorganism in the gastric epithelium. Modulation of the host epithelial antimicrobial responses may be a critical determinant in H. pylori-induced gastritis. Human β-defensins (hBDs) are important components of the host defence at mucosal surfaces. The aim of the present study was to investigate the relevance of three single nucleotide polymorphisms (SNPs) of the human β defensin-1 (hBD-1) gene in H. pylori-induced gastritis and to assess the mRNA expression of hBD-1 in H. pylori-infected AGS cells. Material and methods. Three SNPs of the beta defensin DEFB1 gene, DEFB1 G-20A (rs11362), DEFB1 C-44G (rs1800972) and DEFB1 G-52A (rs1799946), were genotyped either by Custom TaqMan® SNP genotyping assays or by restriction fragment length polymorphism (RFLP) in 150 patients with chronic active gastritis; 100 serologically H. pylori-positive subjects without gastric or duodenal symptoms served as controls. hBD-1 mRNA expression in AGS cells was measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR). Results. Significant differences in frequencies of the GA and AA genotypes of G-52A SNPs were observed between patients with chronic active gastritis and healthy controls. The maximum level of hBD-1 mRNA expression in AGS cells was observed at 24 h after infection with H. pylori, this not being dependent on the presence of the cag pathogenicity island (PAI). Conclusions. The results of these genetic and in vitro experiments suggest that not only the inducible, but also the constitutive form of hBD may be important in the pathogenesis of H. pylori-induced gastritis.