Functional changes induced by psychological stress are not enough to cause intestinal inflammation in Sprague-Dawley rats.

Background: It is well known that stress contributes to the perpetuation of several gastrointestinal diseases. However, its role as a trigger of the inflammatory process in absence of other putative contributing factors remains controversial. Our aim was to elucidate whether stress per se can induce a primary gut inflammation in non-predisposed rats.

Methods: Male Sprague-Dawley rats were divided in sham and stress groups. Chronic stress was induced by subjecting animals 1 h day(-1) to wrap restraint or water avoidance stress alternatively for five consecutive days, as a model of ongoing life stress.

Key Results: Chronic stress induced a significant decrease in body weight gain without changes in food intake and an increase in frequency of defecation. Electromiografic (EMG) study showed that the duration of the migrating motor cycles (MMCs), but not its frequency, was shortened in stressed animals compared with non-stress conditions. Moreover, stressful stimulus caused mucosal mast cell hyperplasia and a decrease of iNOS mRNA expression. Bacterial translocation observed in stressed animals was not related to changes in epithelial barrier function and was not enough to induce intestinal inflammation.

Conclusions & Inferences: Decreased MMC duration, mast cell hyperplasia and decreased mRNA iNOS expression, but not altered epithelial barrier function, could be factors implicated in bacterial translocation-induced by chronic stress. However, these changes are not sufficient to induce intestinal inflammation in stress non-susceptible strain of rats.