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Our in vivo studies performed on vil +/+ and vil / mice by administration of
Dextran Sodium Sulfate (DSS), an abrasive agent of the intestinal epithelium,
have shown a higher probability of death of villin null mice, indicating their
higher susceptibility to cell damage. This allowed us to suggest a role for villin
in epithelial cell plasticity in response to cell injury. This model of intestinal
injury, close to other animal models of rectolitis, could lead, in a long-term
project, to a useful investigation of villin status in human colonic disease such
as Inflammatory Bowel Disease (IBD). A genetic predisposition has been
suggested, and many environmental factors, including bacterial, viral and,
perhaps, dietary antigens, can trigger an ongoing enteric inflammatory
cascade during IBDs. This raises the question of how epithelial cells interact
with components of the immune system and manage to promote the epithelial
mesenchyme transition in response to injury. The investigation of villin
expression levels or mutations in the IBD context can contribute to an
understanding of IBD pathogenesis.
References
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