Helicobacter pylori infection induces interleukin-8 receptor expression in the human gastric epithelium

Abstract

The gastric pathogen Helicobacter pylori is known to activate multiple proinflammatory signaling pathways in epithelial cells. In this study, we addressed the question of whether expression of the interleukin-8 receptors IL-8RA (CXCR1) and IL-8RB (CXCR2) is upregulated in H. pylori-infected human gastric biopsy samples. Biopsy samples from patients infected with H. pylori strains harboring the cag pathogenicity island (PAI) expressed larger amounts of both receptors. In addition, IL-8RB expression was induced in the gastric epithelial cell line AGS upon infection with a clinical isolate containing the cag PAI, while a strain lacking the cag PAI did not. Our finding suggests that gastric epithelial cells express IL-8R in response to H. pylori infection.

FIG. 1.

H. pylori infection induces IL-8R in human biopsy samples. IL-8RA (A) and IL-8RB (B) expression was determined by quantitative real-time RT-PCR for uninfected patients (n = 5), cag PAI-negative strain-infected patients (n = 9), and cag PAI-positive strain-infected patients (n = 6). *, P < 0.05; **, P < 0.01.

FIG.2.

AGS cells express IL-8R. Binding of IL-8 to AGS cells was determined by flow cytometry (solid line). The dashed line shows the background fluorescence of the streptavidin control. These data are representative of three independent experiments.

FIG.3.

Gastric epithelial cells respond to H. pylori infection by expression of IL-8 and IL-8R. AGS cells were infected with H. pylori strain 67:20 (cag PAI negative, white bars) or 67:21 (cag PAI positive, black bars) for 2 or 6 h. IL-8 expression was determined by ELISA (A) and quantitative real-time RT-PCR (B). IL-8RA (C) and IL-8RB (D) expression was determined by quantitative real-time RT-PCR. The values shown are the means ± the standard errors of three independent experiments. *, P < 0.05; **, P < 0.01 (versus cells infected with strain 67:20).