+49 30 838 62550
Background and objectives: Given that only limited information is available about the immunopathogenic properties of Arcobacter infection, we here compared A. butzleri with intestinal pathogenic and commensal species in vivo.
Materials and methods: Gnotobiotic IL10-/- mice were generated by broadspectrum antibiotics and perorally infected with A. butzleri, C. jejuni or a commensal intestinal E. coli strain.
Results: Either strain stably colonized the murine intestines upon infection. At day 6 postinfection, only C. jejuni infected mice displayed clinical sequelae such as wasting bloody diarrhea. Gross disease was accompanied by increased numbers of colonic apoptotic cells and distinct immune cell populations. Whereas A. butzleri and E. coli infected mice were clinically unaffected, colonic immune cell numbers increased in the former, but not in the latter. Both A. butzleri and C. jejuni induced increased secretion of proinflammatory cytokines in large and small intestines. Remarkably, even though viable bacteria did not translocate from the intestines, systemic immune responses were induced in C. jejuni, but also A. butzleri infected mice as indicated by increased pro-inflammatory cytokine concentrations in serum samples.
Conclusion: A. butzleri induce less distinct proinflammatory sequelae as compared to C. jejuni, but more pronounced local and systemic immune responses than commensal E. coli indicating that A. butzleri is more than a commensal in vertebrate hosts.