Increased mast cells in the irritable bowel syndrome

O’Sullivan, Maria; Clayton, Nick M.; Breslin, Niall; Harman, I; Bountra, C; McLaren, Andrew; O’Moráin, Colm

doi:10.1046/j.1365-2982.2000.00221.x

Cited by 422 publications

(354 citation statements)

References 58 publications

Supporting

Mentioning

319

Contrasting

Unclassified

Order By: Relevance

“…Further studies should clarify whether the elimination diet can improve the previously demonstrated mast cell mucosal inflammation and the neural damage which has been reported in IBS. 3,4,[7][8][9] In fact, the relationship between FH and dismotility in pediatric patients has been clearly demonstrated. 20,[33][34][35] ECP might be as useful in FH patients as it is in patients with respiratory allergic diseases.…”

Section: Discussionmentioning

confidence: 99%

Fecal Assays Detect Hypersensitivity to Cow's Milk Protein and Gluten in Adults With Irritable Bowel Syndrome

Carroccio

Brusca

Mansueto

et al. 2011

Clinical Gastroenterology and Hepatology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Fecal Assays Detect Hypersensitivity to Cow's Milk Protein and Gluten in Adults With Irritable Bowel Syndrome

Carroccio

Brusca

Mansueto

et al. 2011

Clinical Gastroenterology and Hepatology

View full text Add to dashboard Cite

“…In support, IBS patients also show increased number and reactivity of mast cells. 28,29 Data from peripheral blood mononuclear cells, as well as in mucosal biopsies, from IBS patients show that cytokines levels including TNF-α, IL-1β and IL-6 are increased in IBS. [30][31][32][33] It is well recognized that proinflammatory cytokines can alter neurotransmitter release within the enteric nervous system to alter motility, secretion, and epithelial permeability via tight junction dysregulation to alter visceral sensitivity.…”

Section: Pathophysiology Of Irritable Bowel Syndrome: Activation Of Tmentioning

confidence: 99%

Mechanisms of Stress-induced Visceral Pain

Meerveld

Johnson

2018

J Neurogastroenterol Motil

View full text Add to dashboard Cite

Evidence suggests that long-term stress facilitates visceral pain through sensitization of pain pathways and promotes chronic visceral pain disorders such as the irritable bowel syndrome (IBS). This review will describe the importance of stress in exacerbating IBS-induced abdominal pain. Additionally, we will briefly review our understanding of the activation of the hypothalamic-pituitary-adrenal axis by both chronic adult stress and following early life stress in the pathogenesis of IBS. The review will focus on the glucocorticoid receptor and corticotropin-releasing hormone-mediated mechanisms in the amygdala involved in stress-induced visceral hypersensitivity. One potential mechanism underlying persistent effects of stress on visceral sensitivity could be epigenetic modulation of gene expression. While there are relatively few studies examining epigenetically mediated mechanisms involved in stress-induced visceral nociception, alterations in DNA methylation and histone acetylation patterns within the brain, have been linked to alterations in nociceptive signaling via increased expression of pro-nociceptive neurotransmitters. This review will discuss the latest studies investigating the long-term effects of stress on visceral sensitivity. Additionally, we will critically review the importance of experimental models of adult stress and early life stress in enhancing our understanding of the basic molecular mechanisms of nociceptive processing. Taken together, the complex clinical phenotype makes recapitulating IBS in rodent models extremely challenging. However, an aim of this review will be to describe how the use of rodent models of adult stress, early life stress (ELS), and a dysregulated HPA axis has improved our understanding of stress in the pathophysiology of IBS. Pathophysiology of Irritable Bowel Syndrome: Activation of the Brain-Gut AxisEvidence from clinical and basic research points to dysregulation of the bidirectional communication between the brain-gut axis in IBS. 21 The brain-gut axis represents a dynamic interplay between central circuits and peripheral mechanisms. The messengers of this complex circuit include neural, endocrine, metabolic, and immune mediators that are activated by central factors such as stress (Fig. 1). Although IBS is not an inflammatory disorder, the immune system plays a role in the pathogenesis of IBS in at least a subset of patients and likely contributes to the etiology of IBS symptoms. 22,23 A subset of IBS patients display a low grade chronic inflammation, and there is also evidence that following an enteric infection and combined with stressful life events, there is an increased risk of developed post-infectious IBS. [24][25][26][27] Clearly, the immune system and inflammatory processes are modulated by the HPA and autonomic nervous systems. In support, IBS patients also show increased number and reactivity of mast cells. 28,29 Data from peripheral blood mononuclear cells, as well as in mucosal biopsies, from IBS patients show that cytokines levels including TNF-α...

show abstract

“…4 MCs hyperplasia and activation lead to abnormal gastrointestinal sensitivity, motility, and secretion, which in turn contribute to the hallmark symptoms of IBS-abdominal pain and/or discomfort, bloating, and abnormal bowel function (diarrhea and/or constipation). 5 Moreover, therapies targeting mast cells, such as mast cell stabilizers (cromoglycate and ketotifen) and antagonists of histamine and serotonin receptors, have been tried in IBS patients in several studies, and partially exhibited good efficacy in symptom improvement. 6,7 It further supported the key role of MCs in the process of IBS.…”

Section: Introductionmentioning

confidence: 99%

Mast Cells and Irritable Bowel Syndrome: From the Bench to the Bedside

Zhang

Song

Hou

2016

J Neurogastroenterol Motil

111

View full text Add to dashboard Cite

Irritable bowel syndrome (IBS) is traditionally defined as a functional disorder since it lacks demonstrable pathological abnormalities. However, in recent years, low grade inflammatory infiltration, often rich in mast cells, in both the small and large bowel, has been observed in some patients with IBS. The close association of mast cells with major intestinal functions, such as epithelial secretion and permeability, neuroimmune interactions, visceral sensation, and peristalsis, makes researchers and gastroenterologists to focus attention on the key roles of mast cells in the pathogenesis of IBS. Numerous studies have been carried out to identify the mechanisms in the development, infiltration, activation, and degranulation of intestinal mast cells, as well as the actions of mast cells in the processes of mucosal barrier disruption, mucosal immune dysregulation, visceral hypersensitivity, dysmotility, and local and central stress in IBS. Moreover, therapies targeting mast cells, such as mast cell stabilizers (cromoglycate and ketotifen) and antagonists of histamine and serotonin receptors, have been tried in IBS patients, and have partially exhibited considerable efficacy. This review focuses on recent advances in the role of mast cells in IBS, with particular emphasis on bridging experimental data with clinical therapeutics for IBS patients.

show abstract

Increased mast cells in the irritable bowel syndrome

Cited by 422 publications

References 58 publications

Fecal Assays Detect Hypersensitivity to Cow's Milk Protein and Gluten in Adults With Irritable Bowel Syndrome

Fecal Assays Detect Hypersensitivity to Cow's Milk Protein and Gluten in Adults With Irritable Bowel Syndrome

Mechanisms of Stress-induced Visceral Pain

Mast Cells and Irritable Bowel Syndrome: From the Bench to the Bedside

Contact Info

Product

Resources

About