A role for vimentin in Crohn disease

Paul Henderson, David Wilson, Jack Satsangi, Craig Stevens*

*Corresponding author for this work

Research output: Contribution to journalEditorialpeer-review

Abstract

Crohn disease (CD), one of the major chronic inflammatory bowel diseases, occurs anywhere in the gastrointestinal tract with discontinuous transmural inflammation. A number of studies have now demonstrated that genetic predisposition, environmental influences and a dysregulated immune response to the intestinal microflora are involved. Major CD susceptibility pathways uncovered through genome-wide association studies strongly implicate the innate immune response (NOD2), in addition to the more specific acquired T cell response (IL23R, ICOSLG) and autophagy (ATG16L1, IRGM). Examination of the disease-associated microbiome, although complex, has identified several potentially contributory microorganisms, most notably adherent-invasive E. coli strains (AIEC), which have been isolated by independent investigators in both adult and pediatric CD patients. Here we discuss our recent finding that the type-III intermediate filament (IF) protein VIM/vimentin is a novel NOD2 interacting protein that regulates NOD2 activities including inflammatory NFKB1 signaling, autophagy and bacterial handling.

Original languageEnglish
Pages (from-to)1695-1696
Number of pages2
JournalAutophagy
Volume8
Issue number11
DOIs
Publication statusPublished - Nov 2012

Keywords

  • AIEC
  • NOD2
  • Crohn disease
  • autophagy
  • vimentin

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