Inflamm Bowel Dis 2016 12;22(12):2824-2839
*Département de Pharmacologie and de Toxicologie, University of Lausanne, Lausanne, Switzerland; Sumedha Malsure is now with the Elanco Animal Health, Basel, Switzerland; and †Institut Universitaire de Pathologie, University Hospital of Lausanne (CHUV), Lausanne, Switzerland.
Background: Inflammatory bowel diseases (IBD) including ulcerative colitis and Crohn's disease are diseases with impaired epithelial barrier function. We aimed to investigate whether mutated prostasin and thus, reduced colonic epithelial sodium channel activity predisposes to develop an experimentally dextran sodium sulfate (DSS)-induced colitis.
Methods: Wildtype, heterozygous (fr/+), and homozygous (fr/fr) prostasin-mutant rats were treated 7 days with DSS followed by 7 days of recovery and analyzed with respect to histology, clinicopathological parameters, inflammatory marker mRNA transcript expression, and sodium transporter protein expression. Read More