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Activation of IL-8 gene expression by Helicobacter pylori is regulated by transcription factor nuclear factor-kappa B in gastric epithelial cells.
J Immunol. 1998 Mar 01; 160(5):2401-7.JI

Abstract

In vivo, gastric infection with Helicobacter pylori leads to substantial production of the inflammatory cytokines IL-1, IL-6, TNF-alpha, and IL-8. H. pylori strains that contain the cag pathogenicity island (cag+) and are associated with ulceration and gastric carcinoma induce greater cytokine production than cag- strains. Expression of these cytokines is often regulated by the transcription factor complex, nuclear factor-kappa B (NF-kappa B) through kappa B-binding elements in the enhancer/promoter regions of their genes. We report that more virulent cag+ H. pylori strains induce increased NF-kappa B-DNA binding activity, which elevates IL-8 expression in AGS gastric epithelial cells. The cag+ H. pylori strains induce significant stimulation of IL-8 promoter-driven reporter activity, while cag- strains do not. Furthermore, mutation of specific genes within the cag island (picA1 and picB) ablates enhanced NF-kappa B activation and IL-8 transcription. Increased IL-8 expression is inhibited by mutation in either the NF-kappa B or NF-IL-6 binding element. The cag+ strains, compared with the cag- strains, induce enhanced nuclear localization of a RelA-containing NF-kappa B binding complex, but no increase in NF-IL-6 binding activity. These studies demonstrate that the ability of different types of H. pylori strains to activate NF-kappa B correlates with their ability to induce IL-8 transcription and indicate a mechanism for the heightened inflammatory response seen in subjects infected with cag+ H. pylori strains.

Authors+Show Affiliations

Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9498783

Citation

Sharma, S A., et al. "Activation of IL-8 Gene Expression By Helicobacter Pylori Is Regulated By Transcription Factor Nuclear Factor-kappa B in Gastric Epithelial Cells." Journal of Immunology (Baltimore, Md. : 1950), vol. 160, no. 5, 1998, pp. 2401-7.
Sharma SA, Tummuru MK, Blaser MJ, et al. Activation of IL-8 gene expression by Helicobacter pylori is regulated by transcription factor nuclear factor-kappa B in gastric epithelial cells. J Immunol. 1998;160(5):2401-7.
Sharma, S. A., Tummuru, M. K., Blaser, M. J., & Kerr, L. D. (1998). Activation of IL-8 gene expression by Helicobacter pylori is regulated by transcription factor nuclear factor-kappa B in gastric epithelial cells. Journal of Immunology (Baltimore, Md. : 1950), 160(5), 2401-7.
Sharma SA, et al. Activation of IL-8 Gene Expression By Helicobacter Pylori Is Regulated By Transcription Factor Nuclear Factor-kappa B in Gastric Epithelial Cells. J Immunol. 1998 Mar 1;160(5):2401-7. PubMed PMID: 9498783.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of IL-8 gene expression by Helicobacter pylori is regulated by transcription factor nuclear factor-kappa B in gastric epithelial cells. AU - Sharma,S A, AU - Tummuru,M K, AU - Blaser,M J, AU - Kerr,L D, PY - 1998/3/14/pubmed PY - 1998/3/14/medline PY - 1998/3/14/entrez SP - 2401 EP - 7 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 160 IS - 5 N2 - In vivo, gastric infection with Helicobacter pylori leads to substantial production of the inflammatory cytokines IL-1, IL-6, TNF-alpha, and IL-8. H. pylori strains that contain the cag pathogenicity island (cag+) and are associated with ulceration and gastric carcinoma induce greater cytokine production than cag- strains. Expression of these cytokines is often regulated by the transcription factor complex, nuclear factor-kappa B (NF-kappa B) through kappa B-binding elements in the enhancer/promoter regions of their genes. We report that more virulent cag+ H. pylori strains induce increased NF-kappa B-DNA binding activity, which elevates IL-8 expression in AGS gastric epithelial cells. The cag+ H. pylori strains induce significant stimulation of IL-8 promoter-driven reporter activity, while cag- strains do not. Furthermore, mutation of specific genes within the cag island (picA1 and picB) ablates enhanced NF-kappa B activation and IL-8 transcription. Increased IL-8 expression is inhibited by mutation in either the NF-kappa B or NF-IL-6 binding element. The cag+ strains, compared with the cag- strains, induce enhanced nuclear localization of a RelA-containing NF-kappa B binding complex, but no increase in NF-IL-6 binding activity. These studies demonstrate that the ability of different types of H. pylori strains to activate NF-kappa B correlates with their ability to induce IL-8 transcription and indicate a mechanism for the heightened inflammatory response seen in subjects infected with cag+ H. pylori strains. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/9498783/Activation_of_IL_8_gene_expression_by_Helicobacter_pylori_is_regulated_by_transcription_factor_nuclear_factor_kappa_B_in_gastric_epithelial_cells_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=9498783 DB - PRIME DP - Unbound Medicine ER -