scholarly journals Mast Cells as Targets for the Therapy of Inflammatory Bowel Disease

1990 ◽  
Vol 4 (7) ◽  
pp. 285-288
Author(s):  
EY Bissonnette ◽  
RC Benyon ◽  
AD Befus
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mast Cell ◽  
Mast Cells ◽  
Bowel Disease ◽  
Inflammatory Responses ◽  
Therapeutic Interventions ◽  
Cell Hyperplasia ◽  
Beneficial Effects ◽  
Inflammatory Bowel ◽  
Multiple Drugs

The etiology and pathogenesis of inflammatory bowel disease (IBD) is poorly understood. However, numerous studies have demonstrated that immunological and inflammatory responses are activated during this disease. A better understanding of these events will help identify appropriate therapeutic interventions. Mast cell hyperplasia is a prominent feature of inflamed intestinal tissue in IBD. Intestinal mast cells are heterogeneous and at least two populations are present in the human intestine. The authors' objective is to explore mast cell properties, activation and mediators that are involved in the induction, maintenance and perpetuation of inflammatory lesions in the intestine. Although some therapies used in IBD can modulate mast cell activities, whether these actions are important in the beneficial effects of the drugs is unknown. Future drug development targeted to the inhibition of mast cells might be of therapeutic value. However, a cascade of different cellular events are involved in IBD development. The complexity of the disease raises difficulties in the development of therapies. Multiple drugs, selective for different phases of the disease or acting on different cells, might be most appropriate, rather than a single, all-encompassing therapeutic agent.

scholarly journals Mucosal Mast Cells in Irritable Bowel Syndrome and Inflammatory Bowel Disease

2005 ◽  
Vol 48 (3-4) ◽  
pp. 163-164 ◽  
Author(s):  
Bilge Tunc ◽  
Levent Filik ◽  
Engin Altıntas ◽  
Nesrin Turhan ◽  
Aysel Ulker ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mast Cell ◽  
Irritable Bowel Syndrome ◽  
Mast Cells ◽  
Bowel Disease ◽  
Mucosal Mast Cell ◽  
Cell Counts ◽  
Mucosal Mast Cells ◽  
Inflammatory Bowel ◽  
Irritable Bowel

Even though exciting progresses have been until now, further studies are necessary to clearly understand the significance of MMC. Mast cells are thought to participate in the pathogenesis of inflammatory bowel disease and irritable bowel syndrome. However, their role in the pathogenesis remains unsettled. The specific aims of this study were to (1) examine mucosal mast cell counts in the cecum in patient with IBS, and IBD (2) compare MMC between the disease groups. We showed increased MMC count in IBS.

scholarly journals Mast cell mediated ion transport in intestine from patients with and without inflammatory bowel disease

Gut ◽  
1997 ◽  
Vol 41 (6) ◽  
pp. 785-792 ◽  
Author(s):  
S E Crowe ◽  
G K Luthra ◽  
M H Perdue
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Ion Transport ◽  
Bowel Disease ◽  
Short Circuit ◽  
Physiological Role ◽  
Cell Numbers ◽  
Inflammatory Bowel

Background—Mast cells have been shown to regulate intestinal ion transport in animal models and normal human colon but their physiological role in human intestinal inflammatory disorders is unknown.Aims—To examine mast cell regulation of ion transport in inflammatory bowel disease (IBD).Subjects and methods—Small and large intestine was obtained from patients with and without IBD undergoing surgical resection. Short circuit current (Isc) responses to rabbit antihuman IgE, histamine, and electrical stimulation were measured in Ussing chambers. Specimens were also examined for mast cell numbers and degree of inflammation.Results—Isc responses to anti-IgE and histamine were smaller in magnitude in IBD compared with non-IBD tissues. In all tissues, anti-IgE Isc responses were reduced by about 80% in chloride free buffer. The histamine H1 receptor antagonist, pyrilamine, decreased anti-IgE responses in non-IBD tissues. Greater inhibition with pyrilamine was seen in IBD small intestine but its effect was less in IBD colon. Histamine pretreatment of non-IBD control tissues reduced anti-IgE responses to levels seen in IBD colon but had no effect in small intestine. Mast cell numbers were greater in IBD compared with non-IBD small intestine while no differences were observed between the colonic groups. Isc responses to anti-IgE were not correlated with the degree of mucosal inflammation.Conclusions—This study provides further evidence that mast cells are capable of mediating alterations of ion transport in human gut but that this regulatory role may be altered in IBD. The data suggest that prior activation of mast cells with release of histamine may account for the reduced secretory response to anti-IgE observed in IBD colonic tissues.

scholarly journals Can We Target Endogenous Anti-inflammatory Responses as a Therapeutic Strategy for Inflammatory Bowel Disease?

2018 ◽  
Vol 24 (10) ◽  
pp. 2123-2134 ◽  
Author(s):  
Ross John Porter ◽  
Caroline Andrews ◽  
Daniel Paul Brice ◽  
Scott Kenneth Durum ◽  
Mairi Hall McLean
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Strategy ◽  
Inflammatory Responses ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

scholarly journals A Personalised Dietary Approach—A Way Forward to Manage Nutrient Deficiency, Effects of the Western Diet, and Food Intolerances in Inflammatory Bowel Disease

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1532 ◽  
Author(s):  
Bobbi B Laing ◽  
Anecita Gigi Lim ◽  
Lynnette R Ferguson
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Nutrient Deficiency ◽  
Pharmaceutical Products ◽  
Western Diet ◽  
Nutritional Deficiencies ◽  
Nutrient Interactions ◽  
Beneficial Effects ◽  
Inflammatory Bowel ◽  
Individualised Treatment

This review discusses the personalised dietary approach with respect to inflammatory bowel disease (IBD). It identifies gene–nutrient interactions associated with the nutritional deficiencies that people with IBD commonly experience, and the role of the Western diet in influencing these. It also discusses food intolerances and how particular genotypes can affect these. It is well established that with respect to food there is no “one size fits all” diet for those with IBD. Gene–nutrient interactions may help explain this variability in response to food that is associated with IBD. Nutrigenomic research, which examines the effects of food and its constituents on gene expression, shows that—like a number of pharmaceutical products—food can have beneficial effects or have adverse (side) effects depending on a person’s genotype. Pharmacogenetic research is identifying gene variants with adverse reactions to drugs, and this is modifying clinical practice and allowing individualised treatment. Nutrigenomic research could enable individualised treatment in persons with IBD and enable more accurate tailoring of food intake, to avoid exacerbating malnutrition and to counter some of the adverse effects of the Western diet. It may also help to establish the dietary pattern that is most protective against IBD.

Enteroids Derived From Inflammatory Bowel Disease Patients Display Dysregulated Endoplasmic Reticulum Stress Pathways, Leading to Differential Inflammatory Responses and Dendritic Cell Maturation

2019 ◽  
Vol 14 (7) ◽  
pp. 948-961 ◽  
Author(s):  
William D Rees ◽  
Martin Stahl ◽  
Kevan Jacobson ◽  
Brian Bressler ◽  
Laura M Sly ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Bowel Disease ◽  
Inflammatory Responses ◽  
Human Colon ◽  
Intestinal Epithelial ◽  
Stress Changes ◽  
Inflammatory Bowel ◽  
Stress Pathway

Abstract Background and Aims Endoplasmic reticulum [ER] stress in intestinal epithelial cells [IECs] contributes to the pathogenesis of inflammatory bowel disease [IBD]. We hypothesized that ER stress changes innate signalling in human IECs, augmenting toll-like receptor [TLR] responses and inducing pro-inflammatory changes in underlying dendritic cells [DCs]. Methods Caco-2 cells and primary human colon-derived enteroid monolayers were exposed to ATP [control stressor] or thapsigargin [Tg] [ER stress inducer], and were stimulated with the TLR5 agonist flagellin. Cytokine release was measured by an enzyme immunoassay. ER stress markers CHOP, GRP78 and XBP1s/u were measured via quantitative PCR and Western blot. Monocyte-derived DCs [moDCs] were cultured with the IEC supernatants and their activation state was measured. Responses from enteroids derived from IBD patients and healthy control participants were compared. Results ER stress enhanced flagellin-induced IL-8 release from Caco-2 cells and enteroids. Moreover, conditioned media activated DCs to become pro-inflammatory, with increased expression of CD80, CD86, MHCII, IL-6, IL-15 and IL-12p70 and decreased expression of CD103 and IL-10. Flagellin-induced IL-8 production correlated with DC activation, suggesting a common stress pathway. Moreover, there were distinct differences in cytokine expression and basal ER stress between IBD and healthy subject-derived enteroid monolayers, suggesting a dysregulated ER stress pathway in IBD-derived enteroids. Conclusions Cellular stress enhances TLR5 responses in IECs, leading to increased DC activation, indicating a previously unknown mechanistic link between epithelial ER stress and immune activation in IBD. Furthermore, dysregulated ER stress may be propagated from the intestinal epithelial stem cell niche in IBD patients.

scholarly journals Clinical Trials for Inflammatory Bowel Disease: Global Guidance During the COVID-19 Pandemic

2020 ◽  
Vol 14 (Supplement_3) ◽  
pp. S815-S819 ◽  
Author(s):  
Walter Reinisch ◽  
Silvio Danese ◽  
Laurent Peyrin-Biroulet ◽  
Edward V Loftus
Keyword(s):  
Inflammatory Bowel Disease ◽  
Clinical Trials ◽  
Severe Acute Respiratory Syndrome ◽  
Bowel Disease ◽  
Principal Investigators ◽  
Modes Of Action ◽  
Global Guidance ◽  
Inflammatory Bowel ◽  
Multiple Drugs

Abstract The severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]-causing coronavirus disease [COVID]-19 pandemic poses major challenges for patients with inflammatory bowel disease [IBD] to be recruited and maintained in clinical trials. However, clinical trials offer patients who have failed multiple drugs access to study medications with alternative modes of action and the potential for relief from inflammation-mediated symptoms. Therefore, the continuation of clinical trials in IBD during the COVID-19 pandemic is important both for participants and for the community of IBD patients, due to the dire need for an expanded therapeutic armamentarium. As the safety of patients in clinical trials is the leading principle, we are providing ten specific rules to guide patients and principal investigators safely through the challenging time.

Anticolitic Effect of Viscum coloratum through Suppression of Mast Cell Activation

2019 ◽  
Vol 47 (01) ◽  
pp. 203-221 ◽  
Author(s):  
Jae-Myung Yoo ◽  
Kwang Il Park ◽  
Jin Yeul Ma
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mast Cell ◽  
Bowel Disease ◽  
Immunoglobulin E ◽  
Janus Kinase ◽  
Mast Cell Activation ◽  
Matrix Metalloprotease ◽  
Zonula Occludens ◽  
Inflammatory Bowel ◽  
Zonula Occludens 1

Viscum coloratum has been used as a component for traditional medicine for therapy of inflammatory diseases. Nonetheless, effect of Viscum coloratum on inflammatory bowel disease is unknown. Therefore, we investigated whether the ethanol extract of Viscum coloratum (VCE) could suppress inflammatory responses in dextran sodium sulfate (DSS)-treated mice and mast cell-derived inflammatory mediator (MDIM)-activated Caco-2 cells. VCE significantly attenuated body weight loss, shortened colon length, enteric epithelium disruption, enterorrhagia and colonic edema in DSS-treated mice. Additionally, VCE decreased the levels of immunoglobulin E, interleukin-6 and tumor necrosis factor-[Formula: see text] in serum and the activity of myeloperoxidase in colonic tissue. Moreover, VCE inhibited the infiltration of immune cells as well as the activity and expression of both matrix metalloprotease-2 and matrix metalloprotease-9. Furthermore, VCE restored zonula occludens-1 expression. Consistent with in vivo studies, VCE suppressed the activity and expression of matrix metalloprotease-2 and matrix metalloprotease-9 in MDIM-activated Caco-2 cells. In addition, VCE reinstated the expression of zonula occludens-1 through inhibiting activation of janus kinase 2/signal transducer and activator of transcription 3 in the cells. In conclusion, VCE exerts anticolitic action through inhibiting the activation of mast cells. Therefore, VCE may be useful as a phytomedicine or functional food for inflammatory bowel disease.

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