Transcriptional regulation by thiol compounds in Helicobacter pylori-induced interleukin-8 production in human gastric epithelial cells

Jeong Yeon Seo, Hye Young Kim, Kyung Hwan Kim

Research output: Contribution to journalArticle

24 Citations (Scopus)


Reactive oxygen species (ROS) have been counted among the potential toxic factors involving Helicobacterpylori (H. pylort) - induced gastric injury. Transcription nuclear factor-κB (NF-κB) 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-κB 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. Leveis of hydrogen peroxide and IL-8 in the medium and DNA binding activity of NF-κB 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-κB activation and IL-8 production induced by H. pylori in AGS cells. In conclusion, ROS may be a signaling molecule triggering NF-κB activation and the expression of inflammatory genes such as IL-8.

Original languageEnglish
Pages (from-to)541-545
Number of pages5
JournalAnnals of the New York Academy of Sciences
Publication statusPublished - 2002 Jan 1


All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this