Motility dysfunction is present in patients with stenotic Crohn’s disease (CD) and contributes to cramps, diarrhea and constipation. However, mechanisms for motility dysfunction in CD are incompletely understood. Mechanical stress, i.e. inflammatory infiltration, edema, stenosis, and distention, is commonly encountered in CD. We tested the hypothesis in a rat model of stenotic CD that mechanical stress-induced expression of mechano-sensitive genes such as cyclo-oxygenase-2 (COX-2) may account for motility dysfunction in the inflammation site and the mechanically distended site prior to inflammation.