Abstract
Campylobacter jejuni and C. coli are typical zoonotic pathogens that are leading causes of bacterial gastroenteritis in humans worldwide. The C. jejuni genome has a high plasticity and the molecular basis for the commensalism in some animals and the expression of virulence in humans is not well understood. C. jejuni colonizes the distal ileum and colon in humans, and ingestion of a few hundred live cells can infect humans. Adherence of C. jejuni to the target cells involves various adhesion factors, and the flagellar export machinery is a crucial secretory device to help C. jejuni entering the host cell. Although the intracellular survival of C. jejuni in non-phagocytic cells has been well documented, there are conflicting reports on the persistence capacity of C. jejuni in phagocytic immune cells. Several animal model systems have been used to study different aspects of this pathogen’s invasion and pathogenicity phases. One of these models shows that the host-specific composition of microbiota is an important determinant in the occurrence of related disease, which complicates even more the study of the interaction of C. jejuni with mammalian host cells. The infant mice model shows promise to be a model system that closely mimics what happens in human cells after invasion by C. jejuni.
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