Background: Stress of different origin is known to alter so called “braingut axis” and contributes to a broad array of gastrointestinal disorders including
inflammatory bowel disease (IBD), irritable bowel syndrome (IBS) and other
functional gastrointestinal diseases. The stressful situations and various stressors
including psychosocial events, heat, hypo- and hyperthermia may worsen the course
of IBD via unknown mechanism. The aims of this paper were to provide an overview
of experimental and clinical evidences that stress activates the brain-gut axis which
results in a mucosal mast cells activation and an increase in the production of
proinflammatory cytokines and other endocrine and humoral mediators.
Methods: Research and online content related to effects of stress on lower bowel
disorders are reviewed and most important mechanisms are delineated.
Results: Brain conveys the neural, endocrine and circulatory messages to the gut via brain-gut axis
reflecting changes in corticotrophin releasing hormone, mast cells activity, neurotransmission at the
autonomic nerves system and intestinal barrier function all affecting the pathogenesis of animal colitis
and human IBD. Stress triggers the hypothalamus-pituitary axis and the activation of the autonomic
nervous system, an increase in cortisol levels and proinflammatory cytokines such as tumor necrosis
factor-alpha, interleukin-8, interleukin-1beta and interleukin-6.
Conclusion: The acute or chronic stress enhances the intestinal permeability weakening of the tight
junctions and increasing bacterial translocation into the intestinal wall. An increased microbial load in the
colonic tissue, excessive cytokine release and a partially blunted immune reactivity in response to stress
result in its negative impact on IBD.