Thermotolerant campylobacters are the most frequent cause of bacterial infection of the lower intestine worldwide. The mechanism of pathogenesis of Campylobacter jejuni comprises four main stages: adhesion to intestinal cells, colonization of the digestive tract, invasion of targeted cells, and toxin production. In response to the high number of cases of human campylobacteriosis, various virulence study models are available according to the virulence stage being analyzed. The aim of this review is to compare the different study models used to look at human disease. Molecular biology tools used to identify genes or proteins involved in virulence mechanisms are also summarized. Despite high cost and limited availability, animal models are frequently used to study digestive disease, in particular to analyze the colonization stage. Eukaryotic cell cultures have been developed because of fewer restrictions on their use and the lower cost of these cultures compared with animal models, and this ex vivo approach makes it possible to mimic the bacterial cell–host interactions observed in natural disease cases. Models are complemented by molecular biology tools, especially mutagenesis and DNA microarray methods to identify putative virulence genes or proteins and permit their characterization. No current model seems to be ideal for studying the complete range of C. jejuni virulence. However, the models available deal with different aspects of the complex pathogenic mechanisms particular to this bacterium.

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