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Background   Campylobacter jejuni  infections constitute serious threats to human health with increasing prevalences worldwide. Our knowledge regarding the molecular mechanisms underlying host–pathogen interactions is still limited. Our group has established a clinical  C. jejuni  infection model based on abiotic IL-10 −/−  mice mimicking key features of human campylobacteriosis. In order to further validate this model for unraveling pathogen-host interactions mounting in acute disease, we here surveyed the immunopathological features of the important  C. jejuni  virulence factors FlaA and FlaB and the major adhesin CadF ( Campylobacter  adhesin to fibronectin), which play a role in bacterial motility, protein secretion and adhesion, respectively.    Methods and results  Therefore, abiotic IL-10 −/−  mice were perorally infected with  C. jejuni  strain 81-176 (WT) or with its isogenic  flaA/B  (Δ flaA/B ) or  cadF  (Δ cadF ) deletion mutants. Cultural analyses revealed that WT and Δ cadF  but not Δ flaA/B  bacteria stably colonized the stomach, duodenum and ileum, whereas all three strains were present in the colon at comparably high loads on day 6 post-infection. Remarkably, despite high colonic colonization densities, murine infection with the Δ flaA/B  strain did not result in overt campylobacteriosis, whereas mice infected with Δ cadF  or WT were suffering from acute enterocolitis at day 6 post-infection. These symptoms coincided with pronounced pro-inflammatory immune responses, not only in the intestinal tract, but also in other organs such as the liver and kidneys and were accompanied with systemic inflammatory responses as indicated by increased serum MCP-1 concentrations following  C. jejuni  Δ cadF  or WT, but not Δ flaA/B  strain infection.    Conclusion  For the first time, our observations revealed that the  C. jejuni  flagellins A/B, but not adhesion mediated by CadF, are essential for inducing murine campylobacteriosis. Furthermore, the secondary abiotic IL-10 −/−  infection model has been proven suitable not only for detailed investigations of immunological aspects of campylobacteriosis, but also for differential analyses of the roles of distinct  C. jejuni  virulence factors in induction and progression of disease.    Electronic supplementary material  The online version of this article (10.1186/s13099-019-0306-9) contains supplementary material, which is available to authorized users.

Immunopathological properties of the Campylobacter jejuni flagellins and the adhesin CadF as assessed in a clinical murine infection model