Proinflammatory Cytokine Gene Expression in Human Gastric Epithelial Cells Induced by Increased Motility of H. pylori

Song, In Sung; Kim, Chung Yong; Jung, Hyun Chae; Kim, Tae Ho; Kim, Jung Mogg; Kim, Joo Sung

Abstract

BACKGROUND AND AIMS: Inflammatory reaction to Helicobacter pylori in the human gastric mucosa could be initially triggered by an array of cytokines expressed in infected gastric epithelial cells, The spiral morphology and flagella of these organisms can increase their velocity in a viscous environment such as methylcellulose solution. The goal of this study was to determine whether modification of H. pylori motility could influence the expression of cytokine genes from gastric epithelial cells infected with H. pylori.
METHODS
Adherent human gastric epithelial cells were cultured and overlaid with methylcellulose solutions of varying viscosity. These epithelial cell layers were inoculated with H. pylori. RNAs were then extracted from the gastric epithelial cells. Various cytokine gene expressions were assessed and quantified using reverse transcription- polymerase chain reaction (RT-PCR) and standard synthetic RNA. Cytokine proteins were measured by enzyme linked immunosorbent assay (ELISA).
RESULTS
Expression of mRNA for interleukin (IL)-8 was upregulated in H. pylori infected gastric epithelial cells overlaid with methylcellulose of 15 centipoise (cp) viscosity. The expression of mRNA for IL-la, IL-8, monocyte chemotactic protein (MCP)-1 and granulocyte macrophage colony stimulating factor (GM-CSF) was also upregu.lated in H. pylori-infected gastric epithelial cells overlaid with methylcellulose solution of the same viscosity. The number of molecules of the expressed cytokine transcripts also paralleled the atnounts of protein secreted from gastric epithelial cells infected with H. pylori.
CONCLUSIONS
These results suggest that methylcellulose solution (simulating mucus layer in vivo) can increase contact of H. pylori with gastric epithelial cells by increasing its motility. Such increase can result in the upregulation of mRNA for proinflammatory cytokines in gastric epithelial cells, and thus, enhance inflammatory reaction at H. pylori- infected sites.