Our protocol to generate a null mutant involved the replacement of the cytochrome P450 coding sequence with an antibiotic resistance gene (kanamycin) by homologous recombination. Two fragments, one upstream (F1 – 447 bp) and one downstream (F2 – 589 bp) of the P450 coding sequence were amplified separately by PCR and combined during the second PCR reaction giving a SmaI site at the junction point of the two DNA fragments. All the PCR reactions

The HT29MTXE12 (E12) cell line harbours an adherent mucus layer, providing a novel technique to model mucosal infection in vitro. In this study, we have characterised the interaction of Campylobacter jejuni with E12 cells and exploited its unique mucus layer to examine the potential efficacy of probiotic treatment to attenuate C. jejuni virulence properties. C. jejuni 81-176 colonised and reproduced in E12 mucus. Adhesion to and internalisation of

The host cell environment can alter bacterial pathogenicity. We employed a combination of cellular and molecular techniques to study the expression of Campylobacter jejuni polysaccharides cocultured with HCT-8 epithelial cells. After two passages, the amount of membrane-bound high-molecular-weight polysaccharide was considerably reduced. Microarray profiling confirmed significant downregulation of capsular polysaccharide (CPS) locus genes. Experiments