Interaction ofCampylobacter jejuniwith Host Cells

This chapter discuss three critical aspects of the interaction of Campylobacter jejuni with host cells: (i) its ability to mediate its own uptake into nonphagocytic cells, (ii) its ability to modulate vesicular trafficking pathways to avoid delivery into lysosomes, and (iii) its ability to reprogram host cell gene expression to stimulate the production of proinflammatory cytokines. The strong phenotype associated with capsular mutants in different animal models is likely to be due to reasons other than their rather minor effect in bacterial internalization. Therefore, it is likely that the capsular polysaccharide may contribute to internalization indirectly, perhaps by promoting bacterial attachment to host cells. Bacterial internalization does not require dynamin, an essential component of the endocytic machinery associated with cavaealoe. Like other intracellular pathogens, C. jejuni must have evolved specific adaptations to survive within host cells. Intestinal epithelial cells are equipped to mount innate immune responses upon detection of microbial pathogens. The last few years have seen advances in the understanding of the cell biology of infection, although more studies will be required to gain an understanding of these issues on par with that of other pathogenic bacteria. Although many C. jejuni mutants apparently defective in some of these process have been identified (e.g., bacterial entry), the direct involvement of these determinants in C. jejuni– host cell interactions has not been demonstrated. The availability of powerful genetic tools, coupled with a better understanding of the cell biology of infection, can help to identify those bacterial determinants.