Interleukin-10 gene-deficient mice develop a primary intestinal permeability defect in response to enteric microflora.

@article{Madsen1999Interleukin10GM,
  title={Interleukin-10 gene-deficient mice develop a primary intestinal permeability defect in response to enteric microflora.},
  author={Karen L Madsen and David Malfair and David Gray and Jason S. G. Doyle and Lawrence D. Jewell and Richard N Fedorak},
  journal={Inflammatory bowel diseases},
  year={1999},
  volume={5 4},
  pages={262-70}
}
The normal intestinal epithelium provides a barrier relatively impermeable to luminal constituents. However, patients with inflammatory bowel disease experience enhanced intestinal permeability that correlates with the degree of injury. IL-10 gene-deficient mice were studied to determine whether increased intestinal permeability occurs as a primary defect before the onset of mucosal inflammation or is secondary to mucosal injury. At 2 weeks of age, IL-10 gene-deficient mice show an increase in… CONTINUE READING