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    Toll-like-Receptor-4 is essential for Arcobacter butzleri induced colonic and systemic immune responses in gnotobiotic IL-10-/- mice (2015)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Gölz, G. (WE 8)
    Karadas, G. (WE 8)
    Fischer, A.
    Göbel, U.B.
    Alter, T. (WE 8)
    Bereswill, S.
    Heimesaat, M.M. (WE 10)
    Quelle
    European journal of microbiology & immunology; 5(4) — S. 321–332
    ISSN: 2062-509x
    Sprache
    Englisch
    Verweise
    URL (Volltext): http://www.akademiai.com/doi/pdf/10.1556/1886.2015.00043
    DOI: 10.1556/1886.2015.00043
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    Institut für Lebensmittelsicherheit und -hygiene

    Königsweg 69
    14163 Berlin
    Tel.+49 30 838 62550 Fax.+49 30 838 46029
    email:lebensmittelhygiene@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Arcobacter butzleri causes sporadic cases of gastroenteritis, but the underlying immunopathological mechanisms of infection are unknown. We have recently demonstrated that A. butzleri-infected gnotobiotic IL-10−/− mice were clinically unaffected but exhibited intestinal and systemic inflammatory immune responses. For the first time, we here investigated the role of Toll-like receptor (TLR)-4, the main receptor for lipopolysaccharide and lipooligosaccharide of Gram-negative bacteria, in murine arcobacteriosis. Gnotobiotic TLR-4/IL-10-double deficient (TLR-4−/− IL-10−/−) and IL-10−/− control mice generated by broad-spectrum antibiotics were perorally infected with A. butzleri. Until day 16 postinfection, mice of either genotype were stably colonized with he pathogen, but fecal bacterial loads were approximately 0.5–2.0 log lower in TLR-4−/− IL-10−/− as compared to IL-10−/− mice. A. butzleriinfected TLR-4−/− IL-10−/− mice displayed less pronounced colonic apoptosis accompanied by lower numbers of macrophages and monocytes, T lymphocytes, regulatory T-cells, and B lymphocytes within the colonic mucosa and lamina propria as compared to IL-10−/− mice. Furthermore, colonic concentrations of nitric oxide, TNF, IL-6, MCP-1, and, remarkably, IFN-γ and IL-12p70 serum levels were lower in A. butzleri-infected TLR-4−/− IL-10−/− versus IL-10−/− mice. In conclusion, TLR-4 is involved in mediating murine A. butzleri infection. Further studies are needed to investigate the molecular mechanisms underlying Arcobacter–host interactions in more detail.