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Background and objectives: Arcobacter butzleri have been shown to cause sporadic cases of human gastroenteritis with abdominal pain and acute or prolonged diarrhea. Information about the underlying immunopathological mechanisms of infection, however, is limited. For the first time we investigated the role of Toll-like-Receptor (TLR) -4, the main innate receptor for lipopolysaccharide and lipooligosaccharide of Gram-negative bacteria, in murine Arcobacter infection.
Materials and methods: Gnotobiotic TLR-4 IL-10 double deficient (TLR-4-/- IL-10-/-) and IL-10-/- control mice were generated by antibiotic treatment and perorally infected with A. butzleri.
Results: Until day 16 postinfection TLR-4-/- IL-10-/- and IL-10-/- control mice were stably colonized by A. butzleri. Infected IL-10-/- mice lacking TLR-4 displayed less pronounced colonic apoptosis that was accompanied by lower numbers of innate and adaptive immune cells within the colonic mucosa and lamina propria as compared to IL-10-/- controls. Furthermore, large intestinal pro-inflammatory mediators including nitric oxide, TNF, IL-6 and MCP-1 and, remarkably, of systemic pro-inflammatory cytokines such as IFN-γ and IL-12p70 were lower in A. butzleri infected TLR-4-/- IL-10-/- compared to IL-10-/- mice.
Conclusion: TLR-4 is involved in mediating Arcobacter infection in vivo. Further studies are needed to investigate the molecular mechanisms underlying arcobacteriosis in more detail.