Novel Salmonella typhimurium properties in host-parasite interactions

Stefan Borg, Johanna Björkman, Sofia Eriksson, Anna Syk, Dan I. Andersson, Kurt Schesser, Mikael Rhen, Sven Pettersson, Neil S. French

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


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 pseudotuberculosis 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. pseudotuberculosis 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.

Original languageEnglish (US)
Pages (from-to)247-249
Number of pages3
JournalImmunology Letters
Issue number2-3
StatePublished - Jun 1 1999
Externally publishedYes


  • NF-κB
  • Salmonella typhimurium
  • Type III secretion system

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy


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