These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Helicobacter pylori-induced expression of interleukin-8 and cyclooxygenase-2 in AGS gastric epithelial cells: mediation by nuclear factor-kappaB.
    Author: Kim H, Lim JW, Kim KH.
    Journal: Scand J Gastroenterol; 2001 Jul; 36(7):706-16. PubMed ID: 11444469.
    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. CONCLUSION: NF-kappaB may play a novel role in expression of IL-8 and COX-2 in H. pylori-induced gastric inflammation.
    [Abstract] [Full Text] [Related] [New Search]