Article

The Effects of Physical and Psychological Stress on the Gastrointestinal Tract: Lessons from Animal Models

Sección de Gastroenterología, Servicio de Aparato Digestivo, Hospital General Universitario "Gregorio Marañón", C/ Dr Esquerdo 46. 28007 Madrid, Spain.
Current Molecular Medicine (Impact Factor: 3.62). 07/2008; 8(4):299-312. DOI: 10.2174/156652408784533751
Source: PubMed

ABSTRACT

Physical and psychological stresses are widely accepted as triggers and / or modifiers of the clinical course of diverse gastrointestinal disorders such as peptic ulcer, irritable bowel syndrome or inflammatory bowel disease. Growing experimental evidence from a variety of models such as immobilization, thermal injury or early maternal deprivation in laboratory animals uniformly supports the ability of stress to induce the development of gastric ulcers, altered gastrointestinal motility and ion secretion, and increased intestinal permeability leading to the passage of antigens to the lamina propria and bacterial translocation. Stress can also synergize with other pathogenic factors such as Helicobacter pylori, non-steroidal anti-inflammatory drugs or colitis-inducing chemicals to produce gastrointestinal disease. The brain-gut axis provides the anatomical basis through emotions and environmental influences modulate the gastrointestinal function through the regulation of gastrointestinal immune system and mucosal inflammation; in this sense, mucosal mast cells - at cellular level - and corticotropin releasing factor (CRF) - at molecular level - seem to play a crucial role. On the other hand, an array of adaptive responses have been evolved in order to maintain the homeostasis and to ensure the survival of the individual. In the gut mucosa anti-inflammatory pathways counteract the deleterious effect of the stressful stimuli on the gastrointestinal homeostasis. In the present review we discuss the several experimental approaches used to mimic human stressful events or chronic stress in laboratory animals, the evidence of stress-induced gastrointestinal inflammation and dysfunction derived from them, and the involved cellular and molecular mechanisms that are being discovered during the last years.

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    • "Corticosterone (rodent)/cortisol (human) exert a negative feedback on the paraventricular nucleus of the hypothalamus and pituitary gland ultimately contributing to the termination of the response (Turnbull and Rivier, 1997). Far beyond an exclusive neuroendocrine role, CRF, which is widely distributed outside of the hypothalamus (De Souza and Grigoriadis, 2002), also acts as a neurotransmitter/ neuromodulator to coordinate the behavioral, autonomic, immune, and visceral efferent limbs of the stress response (Bale and Vale, 2004; Caso et al., 2008; Friedman and Irwin, 1995; Taché et al., 2001). For instance brain CRF activates the sympathetic nervous system inducing the systemic release of catecholamines (adrenaline and noradrenaline) involved in the " fight or flight " response (Tsatsanis et al., 2007; Usui et al., 2009; Yorimitsu et al., 2008). "
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