title: Helicobacter pylori-induced expression of interleukin-8 and cyclooxygenase-2 in AGS gastric epithelial cells: mediation by nuclear factor-kappaB.
abstract: BACKGROUND
  Helicobacter pylori infection might activate nuclear factor-kappaB (NF-kappaB), a transcriptional regulator of inducible expression of inflammatory genes, interleukin-8 (IL-8) and cyclooxygenase-2 (COX-2). We studied the role of NF-kappaB on expression of IL-8 and COX-2 in H. pylori-stimulated AGS gastric epithelial cells by using antisense oligonucleotide (AS ODN) for NF-kappaB subunit p50 and an antioxidant, glutathione (GSH) as well as a NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC).
  
  
  METHODS
  AGS cells were treated with p50 AS ODN, GSH or PDTC in the presence of H. pylori. mRNA expression and protein levels for IL-8 and COX-2 were determined by Northern blot analysis and Western blot analysis. Levels of IL-8, 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) and thromboxane B2 (TXB2) were measured in the medium by enzyme-linked immunosorbent assay. NF-kappaB activation was examined by electrophoretic mobility shift assay.
  
  
  RESULTS
  H. pylori induced a time-dependent expression of mRNA and protein for IL-8 and COX-2 via activation of NF-kappaB and increased the levels of IL-8, 6-keto-PGF1alpha and TXB2, which were inhibited by GSH and PDTC. H. pylori-induced expression of IL-8 and COX-2 was blocked in AGS cells transfected with p50 AS ODN.
  
  
  CONCLUSIONS
  NF-kappaB may play a novel role in expression of IL-8 and COX-2 in H. pylori-induced gastric inflammation.
authors.affiliation: Dept. of Pharmacology and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: H
authors.initials: H
authors.lastname: Kim
authors.forename: J W
authors.initials: JW
authors.lastname: Lim
authors.forename: K H
authors.initials: KH
authors.lastname: Kim
mesh_terms: D000230:Adenocarcinoma / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D000975:Antioxidants / Q000494:pharmacology; D051546:Cyclooxygenase 2; D004353:Drug Evaluation, Preclinical; D004848:Epithelium; D005753:Gastric Mucosa / Q000166:cytology* / Q000276:immunology*; D005756:Gastritis / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects* / Q000276:immunology*; D005978:Glutathione / Q000494:pharmacology; D016481:Helicobacter Infections / Q000150:complications* / Q000276:immunology* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D018928:Immunity, Mucosal; D016209:Interleukin-8 / Q000032:analysis / Q000502:physiology*; D007527:Isoenzymes / Q000032:analysis / Q000187:drug effects* / Q000502:physiology*; D008565:Membrane Proteins; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000187:drug effects* / Q000502:physiology*; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000032:analysis / Q000187:drug effects* / Q000502:physiology*; D011759:Pyrrolidines / Q000494:pharmacology; D013274:Stomach Neoplasms / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D013859:Thiocarbamates / Q000494:pharmacology; D013997:Time Factors; D014158:Transcription, Genetic / Q000187:drug effects / Q000502:physiology; D014407:Tumor Cells, Cultured
chemical_list: D000975:Antioxidants; D016209:Interleukin-8; D007527:Isoenzymes; D008565:Membrane Proteins; D016328:NF-kappa B; D016376:Oligonucleotides, Antisense; D011759:Pyrrolidines; D013859:Thiocarbamates; C020972:pyrrolidine dithiocarbamic acid; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D005978:Glutathione