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Journal Article
Research Support, Non-U.S. Gov't
Transcriptional regulation by thiol compounds in Helicobacter pylori-induced interleukin-8 production in human gastric epithelial cells.
Annals of the New York Academy of Sciences 2002 November
Reactive oxygen species (ROS) have been counted among the potential toxic factors involving Helicobacter pylori (H. pylori)-induced gastric injury. Transcription nuclear factor-kappaB (NF-kappaB) is activated by ROS and regulates inflammatory gene expression. Thiol compounds, such as glutathione and N-acetylcysteine, scavenge hydrogen peroxide and are reported to prevent oxidative damage in various cells. The present study aims to investigate whether thiol compounds could affect H. pylori-induced IL-8 production by regulating transcription factor NF-kappaB in human gastric epithelial AGS cells. AGS cells were incubated with H. pylori (NCTC 11637) at a ratio of 1:100 in the presence or absence of thiol compounds. ROS generation was determined by confocal microscopy using ROS-sensitive dichlorofluorescein diacetate dye. Levels of hydrogen peroxide and IL-8 in the medium and DNA binding activity of NF-kappaB were determined by enzyme-linked immunosorbent assay, colorimetric assay, and electrophoretic mobility shift assay. Results indicated both thiol compounds inhibited H. pylori-induced hydrogen peroxide production, in accordance with their inhibition on NF-kappaB activation and IL-8 production induced by H. pylori in AGS cells. In conclusion, ROS may be a signaling molecule triggering NF-kappaB activation and the expression of inflammatory genes such as IL-8.
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