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    Arcobacter butzleri induces pro-inflammatory immune responses in the intestinal tract of gnotobiotic IL-10-/- mice upon peroral infection (2014)

    Art
    Vortrag
    Autoren
    Gölz, Greta (WE 8)
    Karadas, Gül (WE 8)
    Fischer, André
    Göbel, Ulf B
    Alter, Thomas (WE 8)
    Bereswill, Stefan
    Heimesaat, Markus M
    Kongress
    CARO 2014
    FU-Berlin, Campus Düppel, 20. – 21.11.2014
    Quelle
    Workshop CARO 2014 - Campylobacter, Arcobacter & Related Organisms
    Berlin, 2014 — S. 56–57
    Kontakt
    Institut für Lebensmittelsicherheit und -hygiene

    Königsweg 69
    14163 Berlin
    +49 30 838 62550
    lebensmittelhygiene@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Background
    Arcobacter and Campylobacter are closely related Gram-negative bacterial species. We have recently shown that C. jejuni induces acute ulcerative enterocolitis in gnotobiotic IL-10-/- mice within one week upon peroral infection mimicking key features of severe campylobacteriosis in humans. The parthological relevance of Arcobacter in human gastrointestinal disease, however, is of current debate. Furthermore, in vivo studies investigating the immunopathological impact of A. butzleri in vertebrates are lacking.
    Methodology/Principal Findings
    To address this, gnotobiotic IL-10-/- mice were generated by broad-spectrum antibiotic treatment and perorally challenged with either 10E9 colony forming units (CFU) of A. butzleri strain H1 (isolated from an infected human) or C1 (derived from infected chicken) on two consecutive days. One week following infection with either strain mice harboured the respective A. butzleri strain within the small and large intestines but did not display clinical symptoms such as bloody diarrhea as seen in C. jejuni infected gnotobiotic IL-10-/- mice. Interestingly, pro-inflammatory cytokines such as TNF-, IFN-γ, MCP-1, and IL-6 were higher in ex vivo ileal and colonic biopsies taken from A. butzleri infected as compared to uninfected mice. Interestingly, increases in intestinal cytokine levels upon A. butzleri infection were more pronounced in H1 strain as compared to C1 strain infected mice. We are currently investigating the quantitative abundance of distinct immune cell population in intestinal paraffin sections applying in situ immunohistochemistry. Striking, Arcobacter induced inflammatory responses were not restricted to the intestines given that pro-inflammatory cytokines were also increased in serum samples derived from A. butzleri infected versus naïve mice.
    Conclusion/Significance
    A. butzleri induces intestinal and systemic pro-inflammatory immune responses one week following peroral infection in the gnotobotic IL-10-/- mouse model. Further studies should unravel the immunopathological impact of Arcobacter in humans.