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Comparative Study
. 1999 Nov;5(4):262-70.
doi: 10.1097/00054725-199911000-00004.

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

K L Madsen  1 , D Malfair, D Gray, J S Doyle, L D Jewell, R N Fedorak
Affiliations
Comparative Study

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

K L Madsen et al. Inflamm Bowel Dis. 1999 Nov.

Abstract

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 ileal and colonic permeability in the absence of any histological injury. This primary permeability defect is associated with increased mucosal secretion of interferon-gamma and tumor necrosis factor-alpha, and does not involve an increase in nitric oxide synthase activity. Colonic permeability remains elevated as inflammation progresses, while ileal permeability normalizes by 6 weeks of age. IL-10 gene-deficient mice raised under germ-free conditions have no inflammation, and demonstrate normal permeability and cytokine levels. This data suggests that the intestinal permeability defect in IL-10 gene-deficient mice occurs due to a dysregulated immune response to normal enteric microflora and, furthermore, this permeability defect exists prior to the development of mucosal inflammation.

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