Mechanisms by which Stress Affects the Experimental and Clinical Inflammatory Bowel Disease (IBD): Role of Brain-Gut Axis

Abstract

BackgroundStress of different origin is known to alter so called “brain-gut 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.MethodsResearch and online content related to effects of stress on lower bowel disorders are reviewed and most important mechanisms are delineated.ResultsBrain 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.ConclusionThe 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.

Application of Entropy-Based Metrics to Identify Emotional Distress from Electroencephalographic Recordings

“…Although short-term distress may not be a risk factor for health, chronic negative stress can result in mental diseases like generalized anxiety or depression [39]. Moreover, this emotion can sometimes represent a risk factor for hypertension and coronary artery disease [40] as well as cause or aggravate other physical disorders, such as irritable bowel syndrome, gastroesophageal reflux disease or back pain [41,42]. As a consequence, the present work is completely focused on discerning between the emotional states of calm and negative stress.…”

Brain–Gut Relationship on Mucosal Inflammation in the Gastrointestinal Tract

“…39,41 Stressinduced alterations in IBD may be mediated by activation of HPA axis as well as by disruption of mucosal tight junctions, which results in enhancement of mucosal permeability, facilitation of microbial translocation into the intestinal wall, and development of immune response and inflammation. 50 Moreover, different cytokines (e.g. IL-1b, IL-6, and TNF-a) having a role in the pathogenic mechanism of IBD, directly or indirectly through the formation of PGE 2 promote additional synthesis of cytokines (e.g.…”

“…Thus, stress results in a negative impact on IBD. 50 Change of composition of microflora is recognized as one of the main mechanisms in the pathogenesis of IBD. Dopamine and noradrenaline increased enterohemorrhagic E. coli O157:H7 adherence compared to untreated control tissues in murine cecum under ex vivo condition.…”

EDITORIAL (Thematic Issue: Brain Gut Axis-New View)

“…Based on several lines of evidence, Bartosz Brzozowski, Agnieszka Mazur-Bialy, Robert Pajdo, Slawomir Kwiecien, Jan Bilski, Malgorzata Zwolinska-Wcislo, Tomasz Mach, and Tomasz Brzozowski [1] 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 mediators. In addition, they discuss the concept of acute and chronic stress-induced increased intestinal permeability leading to weakening of the tight junctions and an increased bacterial translocation into the intestinal wall.…”

“…In addition, they discuss the concept of acute and chronic stress-induced increased intestinal permeability leading to weakening of the tight junctions and an increased bacterial translocation into the intestinal wall. An increased microbial load in the colonic tissue, excessive cytokine production and a partially blunted immune response in response to stress may result in inflammation and all these changes have been hypothesized to be involved in developing inflammatory bowel disease [1]. …”