Inflammatory bowel disease (IBD) comprises different diseases in the gastro
intestinal tract in human, of which Crohn's disease (CD) and ulcerative col
itis (UC) are the most prominent. A key factor in the etiology of IBD is th
e chronic inflammatory process, and a large body of evidence suggests that
the transcription factor nuclear factor-kappa B (NF-kappa B) is the key reg
ulator of responses determining the clinical inflammatory condition. Recent
findings using antisense oligonucleotides provide direct evidence that the
p65 subunit of NF-kappa B plays a central role in chronic intestinal infla
mmation. It has previously been shown that the Gram negative bacteria Yersi
nia pseudotubercolosis targets the eukaryotic signal transduction pathway(s
) that lead to NF-kappa B activation (and thus avoid an anti-bacterial infl
ammatory response). In this paper, growth-based selected Salmonella typhimu
rium clones have been used to generate a clearer picture of the molecular m
echanisms involved in host-parasite interactions. From the results presente
d here, S. typhimurium and Y. pseudotubercolosis may use the same mechanism
to block NF-kappa B activation, following host cell infection. A new adapt
ational feature could also be shown, where a growth-based selected bacteria
avoided the normally induced translocation of NF-kappa B in host cells. (C
) 1999 Elsevier Science B.V. All rights reserved.