Mast Cells and Intestinal Motility Disorders (Mastocytic Enteritis/Colitis)

Schaeffer, David F.; Kirsch, Richard; Riddell, Robert H.

doi:10.1007/s10620-012-2123-6

Cited by 4 publications

(4 citation statements)

References 51 publications

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“…Recent studies conducted on this topic suggest that the conclusion of a 5-year-old reviewthat the available evidence does not justify the routine evaluation of MC count in IBS-D biopsies and that this practice should be restricted to research settings [66] would still appear to be valid.…”

Section: Discussionmentioning

confidence: 99%

Mastocytic Enterocolits and the Role of Mast Cells in Functional and Inflammatory Intestinal Disorders: A Systematic Review

Capannolo¹,

Ciccone²,

Latella³

2018

Dig Dis

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Background: Chronic diarrhoea affects 5–10% of the adult population. Histologic lesions of possible diagnostic significance are found under normal colonoscopy in approximately 30% of patients affected by chronic diarrhoea. Mastocytic enterocolitis is characterized by an increase in the number of mucosal mast cells (MC) in the gut of patients with chronic intractable diarrhoea, detected by immunohistochemical staining, responding to mast-cell targeted drugs. The question arises whether to search for MC infiltration in specific subsets of patients as a matter of routine clinical practice. Summary: A systematic electronic search of the English literature up to December 2017 was performed, using Medline, EMBASE, Web of Science, Scopus, and the Cochrane Library. This revealed 9 studies reporting an increased number of MC in the gut mucosa of patients with chronic diarrhoea. No consensus was found, however, on the actual cutoff point, the overlap in range between patients and controls being too great to be of clinical significance. The available evidence does not therefore justify the routine evaluation of MC count. Key Messages: More studies are needed to better define MC count and the significance of MC degranulation in normal and pathological settings. Until these become available, the search for MC infiltration in specific subsets of patients should be restricted to research settings.

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Section: Discussionmentioning

confidence: 99%

Mastocytic Enterocolits and the Role of Mast Cells in Functional and Inflammatory Intestinal Disorders: A Systematic Review

Capannolo¹,

Ciccone²,

Latella³

2018

Dig Dis

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“…There are close apposed between axons and mast cells in the gastrointestinal mucosa ( Stead et al, 1989 ). Mast cells can regulate peristalsis and fluid secretion via bidirectional brain-gut interactions between the ENS and the CNS ( Schaeffer et al, 2012 ). Mast cells can stimulate excitatory neurons and activate the ENS network, and thereby promote powerful propulsive motility ( Wang et al, 2014 ).…”

Section: Gut Motility Patternmentioning

confidence: 99%

Action Mode of Gut Motility, Fluid and Electrolyte Transport in Chronic Constipation

Zhao

Chen

et al. 2021

Front. Pharmacol.

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Chronic constipation is a common gastrointestinal disorder, with a worldwide incidence of 14–30%. It negatively affects quality of life and is associated with a considerable economic burden. As a disease with multiple etiologies and risk factors, it is important to understand the pathophysiology of chronic constipation. The purpose of this review is to discuss latest findings on the roles of gut motility, fluid, and electrolyte transport that contribute to chronic constipation, and the main drugs available for treating patients. We conducted searches on PubMed and Google Scholar up to 9 February 2021. MeSH keywords “constipation”, “gastrointestinal motility”, “peristalsis”, “electrolytes”, “fluid”, “aquaporins”, and “medicine” were included. The reference lists of searched articles were reviewed to identify further eligible articles. Studies focusing on opioid-induced constipation, evaluation, and clinic management of constipation were excluded. The occurrence of constipation is inherently connected to disorders of gut motility as well as fluid and electrolyte transport, which involve the nervous system, endocrine signaling, the gastrointestinal microbiota, ion channels, and aquaporins. The mechanisms of action and application of the main drugs are summarized; a better understanding of ion channels and aquaporins may be helpful for new drug development. This review aims to provide a scientific basis that can guide future research on the etiology and treatment of constipation.

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“…Recent environmental factors (eg, extensive antibiotic use, increased processed-food consumption) may underlie decreases in microbiotic diversity and metabolic capacity, in turn altering the Clinical Therapeutics Aerophagia, angioedema in any segment of the luminal tract, dysphagia (often proximal, possibly due to pharyngeal angioedema), pain/inflammation (often migratory) in one or more segments of the luminal tract (from esophagitis to proctitis) and/or one or more solid organs (eg, hepatitis, pancreatitis), queasiness, nausea, vomiting, diarrhea and/or constipation (often alternating), malabsorption (more often selective micronutrient malabsorption than general protein-calorie malabsorption), ascites either from portal hypertension and/or peritoneal serositis; gastroesophageal reflux disease (often "treatment refractory") and inflammatory/ irritable bowel syndrome are common preexisting diagnoses Genitourinary Inflammation (often migratory) in one or more segments of the luminal tracts (ureteritis, cystitis, urethritis, vaginitis, vestibulitis) and/or one or more solid organs function of MCs which, via their proximity to nervous and endocrine system elements, crucially regulate intestinal permeability, visceral sensitivity, and gastrointestinal motility. [30][31][32][33][34] Among key end-products of microbial fermentation of complex polysaccharides in the distal gut, short-chain fatty acids (SCFAs) (eg, butyrate, propionate, acetate) calorically nourish colonocytes and communicate, via specific cell-surface G-protein receptors, with many host cells, including MCs. 35,36 SCFAs inhibit histone deacetylation, modulating cell function through epigenetic changes (a crucial mechanism for the induction of colonic regulatory forkhead box P3 [FoxP3] þ CD4 þ T cells) [37][38][39] and inhibiting MC histamine release.…”

Section: Interactions Between Human Microbiota and Mast Cellsmentioning

confidence: 99%

“…The most successful diet (FODMAP [fermentable oligosaccharides, disaccharides, monosaccharides, and polyols]) decreases colonic gas and SCFA production. 60 Many studies show increased colonic mucosa MCs in diarrhea-dominant and postinfectious IBS 30,32,[61][62][63][64] and sometimes in constipated IBS. 65 Several small clinical trials suggest roles for MC stabilizers in IBS.…”

Section: Clinical Therapeuticsmentioning

confidence: 99%