Functional changes induced by psychological stress are not enough to cause intestinal inflammation in Sprague–Dawley rats E. JORGE,* J. A. FERNA ´ NDEZ,* R. TORRES,  , à,§ P. VERGARA*, – & M. T. MARTIN*, – *Cell Biology, Physiology and Immunology Department, Universitat Auto ` noma de Barcelona, Bellaterra, Spain  Pharmacology Department, Universitat Auto ` noma de Barcelona, Bellaterra, Spain àPneumology and Respiratory Allergy Department, Hospital Clı ´nic, IDIBAPS, Universitat de Barcelona, Barcelona, Spain §Centro de Investigacio ´ n Biome ´dica en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III Mallorca, Spain –Centro de Investigacio ´ n Biome ´dica en Red de Enfermedades Hepa ´ticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Barcelona, Spain Abstract 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 fac- tors 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 avoid- ance 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 cy- cles (MMCs), but not its frequency, was shortened in stressed animals compared with non-stress condi- tions. Moreover, stressful stimulus caused mucosal mast cell hyperplasia and a decrease of iNOS mRNA expression. Bacterial translocation observed in stres- sed 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. Keywords bacterial translocation, chronic stress, inflammation, small intestinal motility. INTRODUCTION Responses induced by stress represent an adaptive mechanism whose objective is to ensure the stability of the internal environment. However, chronic or excessive stress can turn these adaptive mechanisms into contributing factors to initiate or reactivate sev- eral diseases. Regarding gastrointestinal function, changes in motor activity, such as gastric emptying inhibition or increased colonic motility, occur in response to several stressors. 1 Moreover, stress has a great impact on epithelial barrier function, causing an increase in intestinal permeability that can result in an enhanced uptake of macromolecules. 2 This fact may allow an abnormal presentation of luminal constitu- ents to the mucosal immune system and initiate an inflammatory response. Irritable bowel syndrome (IBS) is known as one of stress-related disorders. 3 It is characterized by visceral hypersensitivity and altered gastrointestinal motor activity in the absence of detectable organic abnormal- ities. Although its pathophysiology is far from under- stood, it has been postulated that IBS arises from a dysfunctional brain–gut axis 4,5 and several reports Address for correspondence Maria Teresa Martin, Unitat de Fisiologia (Edifici V), Universitat Auto ` noma de Barcelona, 08193 Bellaterra, Spain. Tel: +34 93 5813834; fax: +34 93 5812006; e-mail: maite.martin@uab.cat Received: 8 September 2009 Accepted for publication: 25 March 2010 Neurogastroenterol Motil (2010) 22, e241–e250 doi: 10.1111/j.1365-2982.2010.01507.x Ó 2010 Blackwell Publishing Ltd e241