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    Modulation of pathogen-induced CCL20 secretion from HT-29 human intestinal epithelial cells by commensal bacteria.

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    Authors
    Sibartie, Shomik
    O'Hara, Ann M
    Ryan, Jude
    Fanning, Aine
    O'Mahony, Jim
    O'Neill, Shaun
    Sheil, Barbara
    O'Mahony, Liam
    Shanahan, Fergus
    Affiliation
    Alimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland. shomiksibartie@gmail.com
    Issue Date
    2009
    MeSH
    Bacteria
    Bacterial Infections
    Chemokine CCL20
    Enzyme-Linked Immunosorbent Assay
    Flagellin
    Gene Expression Regulation
    HT29 Cells
    Host-Pathogen Interactions
    Humans
    Immunity, Mucosal
    Immunomodulation
    Interleukin-8
    Intestinal Mucosa
    NF-kappa B
    Transcriptional Activation
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    Citation
    Modulation of pathogen-induced CCL20 secretion from HT-29 human intestinal epithelial cells by commensal bacteria. 2009, 10:54 BMC Immunol.
    Journal
    BMC immunology
    URI
    http://hdl.handle.net/10147/107596
    DOI
    10.1186/1471-2172-10-54
    PubMed ID
    19814810
    Abstract
    BACKGROUND: Human intestinal epithelial cells (IECs) secrete the chemokine CCL20 in response to infection by various enteropathogenic bacteria or exposure to bacterial flagellin. CCL20 recruits immature dendritic cells and lymphocytes to target sites. Here we investigated IEC responses to various pathogenic and commensal bacteria as well as the modulatory effects of commensal bacteria on pathogen-induced CCL20 secretion. HT-29 human IECs were incubated with commensal bacteria (Bifidobacterium infantis or Lactobacillus salivarius), or with Salmonella typhimurium, its flagellin, Clostridium difficile, Mycobacterium paratuberculosis, or Mycobacterium smegmatis for varying times. In some studies, HT-29 cells were pre-treated with a commensal strain for 2 hr prior to infection or flagellin stimulation. CCL20 and interleukin (IL)-8 secretion and nuclear factor (NF)-kappaB activation were measured using enzyme-linked immunosorbent assays. RESULTS: Compared to untreated cells, S. typhimurium, C. difficile, M. paratuberculosis, and flagellin activated NF-kappaB and stimulated significant secretion of CCL20 and IL-8 by HT-29 cells. Conversely, B. infantis, L. salivarius or M. smegmatis did not activate NF-kappaB or augment CCL20 or IL-8 production. Treatment with B. infantis, but not L. salivarius, dose-dependently inhibited the baseline secretion of CCL20. In cells pre-treated with B. infantis, C. difficile-, S. typhimurium-, and flagellin-induced CCL20 were significantly attenuated. B. infantis did not limit M. Paratuberculosis-induced CCL20 secretion. CONCLUSION: This study is the first to demonstrate that a commensal strain can attenuate CCL20 secretion in HT-29 IECs. Collectively, the data indicate that M. paratuberculosis may mediate mucosal damage and that B. infantis can exert immunomodulatory effects on IECs that mediate host responses to flagellin and flagellated enteric pathogens.
    Language
    en
    ISSN
    1471-2172
    ae974a485f413a2113503eed53cd6c53
    10.1186/1471-2172-10-54
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