Psychological aspects of inflammatory bowel disease

Hisamatsu, Tadakazu; Inoue, Nagamu; Yajima, Tomoharu; Izumiya, Motoko; Ichikawa, Hitoshi; Hibi, Toshifumi

doi:10.1007/s00535-006-1937-4

Cited by 25 publications

(27 citation statements)

References 63 publications

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Section: Role Of Psychological Stress In Ibdmentioning

confidence: 99%

“…Thus, while the role of stress in the onset of IBD has not been established, there is no doubt that stress is a triggering and exacerbating factor in relation to the course and symptoms of IBD [8, 10, 12, 13]. Indeed it can be considered as one of the determinants of disease relapse [12, 14, 15]. However, there are some discordant reports about a relation between stress and disease onset, like that of Li et al [16] who, based on a follow-up study on the onset of IBD in parents who lost a child in Denmark, found a negative relationship between psychological stress and development of IBD.…”

Section: Role Of Psychological Stress In Ibdmentioning

confidence: 99%

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Psychological Issues in Inflammatory Bowel Disease: An Overview

Sajadinejad

Asgari

Molavi

et al. 2012

Gastroenterology Research and Practice

185

140

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Inflammatory bowel disease (IBD) including Crohn's disease (CD) and ulcerative colitis (UC) is a chronic and disabling disease with unknown etiology. There have been some controversies regarding the role of psychological factors in the course of IBD. The purpose of this paper is to review that role. First the evidence on role of stress is reviewed focusing on perceived stress and patients' beliefs about it in triggering or exacerbating the course of IBD. The possible mechanisms by which stress could be translated into IBD symptoms, including changes in motor, sensory and secretory gastrointestinal function, increase intestinal permeability, and changes in the immune system are, then reviewed. The role of patients' concerns about psychological distress and their adjustment to disease, poor coping strategies, and some personality traits that are commonly associated with these diseases are introduced. The prevalence rate, the timing of onset, and the impact of anxiety and depression on health-related quality of life are then reviewed. Finally issues about illness behavior and the necessity of integrating psychological interventions with conventional treatment protocols are explained.

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Section: Role Of Psychological Stress In Ibdmentioning

confidence: 99%

Section: Role Of Psychological Stress In Ibdmentioning

confidence: 99%

Psychological Issues in Inflammatory Bowel Disease: An Overview

Sajadinejad

Asgari

Molavi

et al. 2012

Gastroenterology Research and Practice

185

140

View full text Add to dashboard Cite

show abstract

“…Epidemiology works support the adverse influence of stress in the development and/or aggravation of gastrointestinal disorders such as inflammatory bowel disease (IBD) and colon cancer [2][3][4][5][6] . Colitis associated cancer (CAC) is a subtype of colon cancer that is preceded by clinically detectable IBD.…”

Section: Introductionmentioning

confidence: 99%

A crosstalk between muscarinic and CRF2 receptors regulates cellular adhesion properties of human colon cancer cells

Pelissier-Rota

Chartier

Bonaz

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Patients with inflammatory bowel disease often suffer from chronic and relapsing intestinal inflammation that favor the development of colitis associated cancer. An alteration of the epithelial intestinal barrier function observed in IBD is supposed to be a consequence of stress. It has been proposed that corticotrophin-releasing factor receptor (CRF2), one of the two receptors of CRF, the principal neuromediator of stress, acts on cholinergic nerves to induce stress-mediated epithelial barrier dysfunction. Non-neuronal acetylcholine (Ach) and muscarinic receptors (mAchR) also contribute to alterations of epithelial cell functions. In this study, we investigated the mechanisms through which stress and Ach modulate epithelial cell adhesive properties. We show that Ach-induced activation of mAchR in HT-29 cells results in cell dissociation together with changes in cell-matrix contacts, which correlates with the acquisition of invasive potential consistent with a matrix metalloproteinase (MMP) mode of invasion. These processes result from mAchR subsequent stimulation of the cascade of src/Erk and FAK activation. Ach-induced secretion of laminin 332 leads to α3β1 integrin activation and RhoA-dependent reorganization of the actin cytoskeleton. We show that Ach-mediated effects on cell adhesion are blocked by astressin 2b, a CRF2 antagonist, suggesting that Ach action depends partly on CRF2 signaling. This is reinforced by the fact that Ach-mediated activation of mAchR stimulates both the synthesis and the release of CRF2 ligands in HT-29 cells (effects blocked by atropine). In summary, our data provides evidence for a novel intracellular circuit involving mAchR acting on CRF2-signaling that could mediate colonic mucosal barrier dysfunction and exacerbate mucosal inflammation.

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“…ACTH finally stimulates glucocorticoid secretion by the adrenal cortex (Mawdsley and Rampton, 2005; Kyrou and Tsigos, 2009). Stress is known to aggravate gastrointestinal (GI) disorders, such as Crohn's disease (CD), ulcerative colitis (UC), and irritable bowel syndrome (IBS; Mawdsley and Rampton, 2005; Hisamatsu et al, 2007). CD and UC have a clear inflammatory component and hence are classified as inflammatory bowel diseases (IBD).…”

Section: Introductionmentioning

confidence: 99%

“…The cause of symptoms of IBS patients, however, is not clear. Several epidemiological studies have dealt with the influence of (psychological) stress on GI disorders, but interpretation is difficult due to considerable variation in study design and quality (Mawdsley and Rampton, 2005; Hisamatsu et al, 2007; Musial et al, 2008; Camara et al, 2009; Zijdenbos et al, 2009). However, several in vitro and in vivo studies indicate a clear influence of CRF and related peptides on GI functions and inflammation.…”

Section: Introductionmentioning

confidence: 99%

Corticotrophin-Releasing Factor, Related Peptides, and Receptors in the Normal and Inflamed Gastrointestinal Tract

et al. 2011

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Corticotrophin-releasing factor (CRF) is mainly known for its role in the stress response in the hypothalamic–pituitary–adrenal axis. However, increasing evidence has revealed that CRF receptor signaling has additional peripheral effects. For instance, activation of CRF receptors in the gastrointestinal tract influences intestinal permeability and motility. These receptors, CRF1 and CRF2, do not only bind CRF, but are also activated by urocortins. Most interestingly, CRF-related signaling also assumes an important role in inflammatory bowel diseases in that it influences inflammatory processes, such as cytokine secretion and immune cell activation. These effects are characterized by an often contrasting function of CRF1 and CRF2. We will review the current data on the expression of CRF and related peptides in the different regions of the gastrointestinal tract, both in normal and inflamed conditions. We next discuss the possible functional roles of CRF signaling in inflammation. The available data clearly indicate that CRF signaling significantly influences inflammatory processes although there are important species and inflammation model differences. Although further research is necessary to elucidate this apparently delicately balanced system, it can be concluded that CRF-related peptides and receptors are (certainly) important candidates in the modulation of gastrointestinal inflammation.

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Psychological aspects of inflammatory bowel disease

Cited by 25 publications

References 63 publications

Psychological Issues in Inflammatory Bowel Disease: An Overview

Psychological Issues in Inflammatory Bowel Disease: An Overview

A crosstalk between muscarinic and CRF2 receptors regulates cellular adhesion properties of human colon cancer cells

Corticotrophin-Releasing Factor, Related Peptides, and Receptors in the Normal and Inflamed Gastrointestinal Tract

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