Despite the socioeconomic burden of campylobacteriosis, our insights into the molecular mechanisms underlying Campylobacter (C.) jejuni-induced intestinal immunopathogenesis are limited.The absence and the ban of convenient murine infection models caused fundamental restrictions in Campylobacter research. The development of novel and modified murine infection models in the last years has greatly contributed to our knowledge in Cjejuni--host interactions and pathogenicity. Novel findings revealed that the colonization resistance of mice against C. jejuni infection can be overcome by modification of the intestinal microbiota. In particular C. jejuni infected infant mice harbouring a conventional microbiota and Interleukin-10-deficient mice rendered gnotobiotic by antibiotic treatment develop lipooligosaccharide mediated inflammation and specific T-cell responses--both key features of campylobacteriosis in humans. This short review focuses on the major progress in this growing research field and intends to summarize some of the most important findings.