Fachbereich Veterinärmedizin



    Arcobacter butzleri induce inflammatory responses in IL-10 deficient gnotobiotic mice (2015)

    Gölz, G. (WE 8)
    Karadas, G. (WE 8)
    Alter, T. (WE 8)
    Bereswill, S.
    Heimesaat, M.M. (WE 10)
    Campylobacter, Helicobacter & Related Organisms (CHRO) 2015 : 18th International Workshop
    Rotorua, New Zealand, 01. – 05.11.2015
    Campylobacter, Helicobacter & Related Organisms (CHRO) 2015 : 18th International Workshop, 1-5 November, 2015, Rotorua, New Zealand : Delegate Handbook — CHRO Conference 2015 (Hrsg.)
    Rotorua, New Zealand, 2015 — S. 139
    ISBN: 978-0-473-34059-9
    URL (Volltext): http://chro2015.com/files/CHRO_Guidebook.pdf
    Institut für Lebensmittelsicherheit und -hygiene

    Königsweg 69
    14163 Berlin
    +49 30 838 62550

    Abstract / Zusammenfassung

    Background: Acute gascroenteritis with abdominal pain and acute or prolonged watery diarrhoea has been described for humans infected with Arcobacter (A) butzleri. Adhesive, invasive and cytotoxic capacities have been described for A. buczleri in vitro. So far, only limited information is available about the immune-pathogenic mechanisms of infection in vivo. Objective: The aim of this study was to investigate the immune-pathological properties of A. butzleri in a well-established munne infection model, reflecting major clinical aspects of human campylobacteriosis.
    Methods: Gnotobiotic IL-10-/- mice, achieved by broad-spectrum antibiotic treatment of conventionally raised mice, were orally infected with two different A. butzleri strains and clinical signs as well as fecal shedding were determined over time. At day 6 and day 16 post-infection apoptotic and proliferating cells, intestinal infiltration with immune cells and cytokine expression patterns were determined.
    Results: Despite no overt macroscopic signs of disease, stable infection of IL-10-/- gnotobiotic mice with A. butzleri led to increased numbers of apoptotic cells, influx of immune cells and higher expression of proinflammatory cytokines in the intestine, depending on the respective A. burzleri strain. For instance host responses were delayed after infection with strain C1 as compared to the H1 strain.
    Conclusion: Even though no overt clinical signs have been observed we could clearly show that A. butzleri is able to stably colonize and induce apoptosis paralleled by induction of pro-inflammatory immune responses in the intestine of infected IL-10-/- gnotobiotic mice, pointing towards an immune pathogenic potential of A. buczleri in vivo.