Abnormal CEACAM6 expression in Crohn disease patients favors gut colonization and inflammation by adherent-invasive E. coli

Virulence. Jul-Aug 2010;1(4):281-2. doi: 10.4161/viru.1.4.11510.

Abstract

Abnormal expression of CEACAM6 is observed at the apical surface of the ileal epithelium in Crohn's disease (CD) patients, and CD ileal lesions are colonized by pathogenic adherent-invasive Escherichia coli (AIEC). The paper of Carvalho et al. recently reported that CD associated AIEC colonize and induce strong gut inflammation in transgenic mice expressing human CEACAM6 acting as a receptor for type 1 pili produced by AIEC bacteria. AIEC also induce CEACAM6 expression by intestinal epithelial cells directly by adhering to host cells and indirectly via increased secretion of TNF-α from AIEC-infected macrophages. Patients expressing a basal level of CEACAM6 in ileum could be predisposed to develop ileal CD and blocking interaction between type 1 pili and CEACAM6 might serve as a specific means of disrupting the colonization and the subsequent inflammatory amplification loop.

MeSH terms

  • Animals
  • Antigens, CD / genetics
  • Antigens, CD / metabolism*
  • Bacterial Adhesion
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism*
  • Crohn Disease / immunology
  • Crohn Disease / microbiology*
  • Escherichia coli / growth & development
  • Escherichia coli / pathogenicity*
  • Fimbriae, Bacterial / metabolism
  • GPI-Linked Proteins / genetics
  • GPI-Linked Proteins / metabolism
  • Humans
  • Ileum / metabolism
  • Ileum / microbiology*
  • Inflammation / immunology
  • Inflammation / microbiology
  • Mice
  • Mice, Transgenic
  • Virulence

Substances

  • Antigens, CD
  • CEACAM6 protein, human
  • Cell Adhesion Molecules
  • GPI-Linked Proteins