• Admin Login
    View Item 
    •   Home
    • Faculty of Education, Health and Wellbeing
    • Faculty of Education, Health and Wellbeing
    • View Item
    •   Home
    • Faculty of Education, Health and Wellbeing
    • Faculty of Education, Health and Wellbeing
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of WIRECommunitiesTitleAuthorsIssue DateSubmit DateSubjectsTypesJournalDepartmentPublisherThis CollectionTitleAuthorsIssue DateSubmit DateSubjectsTypesJournalDepartmentPublisher

    Administrators

    Admin Login

    Local Links

    AboutThe University LibraryOpen Access Publications PolicyDeposit LicenceCOREWIRE Copyright and Reuse Information

    Statistics

    Display statistics

    Differential activation of mitogen-activated protein kinases in AGS gastric epithelial cells by cag+ and cag- Helicobacter pylori.

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    Joanne Flavell article.pdf
    Size:
    928.6Kb
    Format:
    PDF
    Download
    Average rating
     
       votes
    Cast your vote
    You can rate an item by clicking the amount of stars they wish to award to this item. When enough users have cast their vote on this item, the average rating will also be shown.
    Star rating
     
    Your vote was cast
    Thank you for your feedback
    Authors
    Keates, Sarah
    Keates, Andrew C.
    Warny, Michel
    Peek, Richard M.
    Murray, Paul G.
    Kelly, Ciaran P.
    Issue Date
    1999
    Submitted date
    2007-01-29
    
    Metadata
    Show full item record
    Abstract
    The aim of this study was to determine whether Helicobacter pylori activates mitogen-activated protein (MAP) kinases in gastric epithelial cells. Infection of AGS cells with an H. pylori cag+ strain rapidly (5 min) induced a dose-dependent activation of extracellular signal-regulated kinases (ERK), p38, and c-Jun N-terminal kinase (JNK) MAP kinases, as determined by Western blot analysis and in vitro kinase assay. Compared with cag+ strains, cag- clinical isolates were less potent in inducing MAP kinase, particularly JNK and p38, activation. Isogenic inactivation of the picB region of the cag pathogenicity island resulted in a similar loss of JNK and p38 MAP kinase activation. The specific MAP kinase inhibitors, PD98059 (25 microM; MAP kinase kinase (MEK-1) inhibitor) and SB203580 (10 microM; p38 inhibitor), reduced H. pylori-induced IL-8 production in AGS cells by 78 and 82%, respectively (p < 0.01 for each). Both inhibitors together completely blocked IL-8 production (p < 0.001). However, the MAP kinase inhibitors did not prevent H. pylori-induced IkappaBalpha degradation or NF-kappaB activation. Thus, H. pylori rapidly activates ERK, p38, and JNK MAP kinases in gastric epithelial cells; cag+ isolates are more potent than cag- strains in inducing MAP kinase phosphorylation and gene products of the cag pathogenicity island are required for maximal MAP kinase activation. p38 and MEK-1 activity are required for H. pylori-induced IL-8 production, but do not appear to be essential for H. pylori-induced NF-kappaB activation. Since MAP kinases regulate cell proliferation, differentiation, programmed death, stress, and inflammatory responses, activation of gastric epithelial cell MAP kinases by H. pylori cag+ strains may be instrumental in inducing gastroduodenal inflammation, ulceration, and neoplasia.
    Citation
    The Journal of Immunology, 163(10): 5552-5559
    Publisher
    American Association of Immunologists
    URI
    http://hdl.handle.net/2436/8018
    PubMed ID
    10553083
    Additional Links
    http://www.jimmunol.org/cgi/reprint/163/10/5552
    Type
    Journal article
    Language
    en
    ISSN
    0022-1767
    1550-6606
    Collections
    Faculty of Education, Health and Wellbeing

    entitlement

    Related articles

    • Mitogen-activated protein kinases and nuclear factor-kappaB regulate Helicobacter pylori-mediated interleukin-8 release from macrophages.
    • Authors: Bhattacharyya A, Pathak S, Datta S, Chattopadhyay S, Basu J, Kundu M
    • Issue date: 2002 Nov 15
    • α-Lipoic Acid Inhibits Expression of IL-8 by Suppressing Activation of MAPK, Jak/Stat, and NF-κB in H. pylori-Infected Gastric Epithelial AGS Cells.
    • Authors: Choi JH, Cho SO, Kim H
    • Issue date: 2016 Jan
    • Regulation of interleukin-6 promoter activation in gastric epithelial cells infected with Helicobacter pylori.
    • Authors: Lu H, Wu JY, Kudo T, Ohno T, Graham DY, Yamaoka Y
    • Issue date: 2005 Oct
    • Helicobacter pylori and mitogen-activated protein kinases regulate the cell cycle, proliferation and apoptosis in gastric epithelial cells.
    • Authors: Ding SZ, Smith MF Jr, Goldberg JB
    • Issue date: 2008 Jul
    • Beta-carotene inhibits Helicobacter pylori-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in human gastric epithelial AGS cells.
    • Authors: Jang SH, Lim JW, Kim H
    • Issue date: 2009 Dec

    DSpace software (copyright © 2002 - 2021)  DuraSpace
    Quick Guide | Contact Us
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.