Novel Salmonella typhimurium properties in host–parasite interactions

Inflammatory bowel disease (IBD) comprises different diseases in the gastrointestinal tract in human, of which Crohn’s disease (CD) and ulcerative colitis (UC) are the most prominent. A key factor in the etiology of IBD is the chronic inflammatory process, and a large body of evidence suggests that the transcription factor nuclear factor-kappa B (NF-κB) is the key regulator of responses determining the clinical inflammatory condition. Recent findings using antisense oligonucleotides provide direct evidence that the p65 subunit of NF-κB plays a central role in chronic intestinal inflammation. It has previously been shown that the Gram negative bacteria Yersinia pseudotubercolosis targets the eukaryotic signal transduction pathway(s) that lead to NF-κB activation (and thus avoid an anti-bacterial inflammatory response). In this paper, growth-based selected Salmonella typhimurium clones have been used to generate a clearer picture of the molecular mechanisms involved in host–parasite interactions. From the results presented here, S. typhimurium and Y. pseudotubercolosis may use the same mechanism to block NF-κB activation, following host cell infection. A new adaptational feature could also be shown, where a growth-based selected bacteria avoided the normally induced translocation of NF-κB in host cells.