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-kappaB) 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-kappaB 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-kappaB 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-kappaB 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-kappaB in host cells.