Background: In inflammatory bowel disease a defective mucosal barrier, a dysregulated
immune response and an excessive reactivity against the gut microbiota are assumed to cause
a breakdown of the intestinal homeostasis and lead to chronic inflammation. Piroxicam
treatment is a method for induction of colitis in IL-10 k.o. mice, which integrates a dysfunction
of both the intestinal barrier and the immune system. However, the translational value of this
model has not been thoroughly clarified.
Aim: To characterise the piroxicam-accelerated colitis (PAC) IL-10 k.o. model with respect to
clinical features, pathogenic mechanisms and its ability to respond to existing therapies.
Methods: The PAC IL-10 k.o. model was established on a C57BL/6 J background and the clinical
manifestations, immunological mechanisms and efficacy of ampicillin and anti-IL-12/23p40
treatment were assessed.