scholarly journals The Effect of Tong-Xie-Yao-Fang on Intestinal Mucosal Mast Cells in Postinfectious Irritable Bowel Syndrome Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiangxue Ma ◽  
Xiaoge Wang ◽  
Nan Kang ◽  
Ting Chen ◽  
Haijie Ji ◽  
...  
Keyword(s):  
Mast Cell ◽  
Irritable Bowel Syndrome ◽  
Mast Cells ◽  
Intestinal Mucosa ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Mucosal Mast Cells ◽  
Fos Expression ◽  
Irritable Bowel ◽  
Postinfectious Irritable Bowel Syndrome

Objective. To investigate the effects of Tong-Xie-Yao-Fang (TXYF) on intestinal mucosal mast cells in rats with postinfectious irritable bowel syndrome (PI-IBS).Design. PI-IBS rat models were established using a multistimulation paradigm. Then, rats were treated with TXYF intragastrically at doses of 2.5, 5.0, and 10.0 g·kg−1·d−1for 14 days, respectively. Intestinal sensitivity was assessed based on abdominal withdrawal reflex (AWR) scores and fecal water content (FWC). Mast cell counts and the immunofluorescence of tryptase and c-Fos in intestinal mucosa were measured; and serum IL-1β, TNF-α, and histamine levels were determined.Results. AWR reactivity and FWC which were significantly increased could be observed in PI-IBS rats. Remarkably increased mast cell activation ratio in intestinal mucosa, together with increased serum TNF-αand histamine levels, could also be seen in PI-IBS rats; furthermore, PI-IBS-induced changes in mast cell activation and level of serum TNF-αand histamine could be reversed by TXYF treatment. Meanwhile, tryptase and c-Fos expression were also downregulated.Conclusion. TXYF improves PI-IBS symptoms by alleviating behavioral hyperalgesia and antidiarrhea, the underlying mechanism of which involves the inhibitory effects of TXYF on activating mucosal mast cells, downregulating tryptase and c-Fos expression, and reducing serum TNF-αand histamine levels.

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 Role of mucosal mast cells in early vascular permeability changes of intestinal DTH reaction in the rat

1998 ◽  
Vol 274 (5) ◽  
pp. G832-G839 ◽  
Author(s):  
Aletta D. Kraneveld ◽  
Thea Muis ◽  
Andries S. Koster ◽  
Frans P. Nijkamp
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Vascular Leakage ◽  
Mast Cell Activation ◽  
Mucosal Mast Cell ◽  
Mucosal Mast Cells

Previously, it was shown that depletion and stabilization of the mucosal mast cell around the time of challenge were very effective in reducing delayed-type hypersensitivity (DTH) reactions in the small intestine of the rat. The role of mucosal mast cells in the early component of intestinal DTH reaction was further investigated in this study. In vivo small intestinal vascular leakage and serum levels of rat mast cell protease II (RMCP II) were determined within 1 h after intragastric challenge of rats that had been sensitized with dinitrobenzene 5 days before. A separate group of rats was used to study vasopermeability in isolated vascularly perfused small intestine after in vitro challenge. To investigate the effects of mast cell stabilization on the early events of the DTH reaction, doxantrazole was used. The influence of sensory nerves was studied by means of neonatal capsaicin-induced depletion of sensory neuropeptides. Within 1 h after challenge, a significant increase in vascular permeability was found in vivo as well as in vitro. This was associated with a DTH-specific increase in RMCP II in the serum, indicating mucosal mast cell activation. In addition, doxantrazole treatment and caspaicin pretreatment resulted in a significant inhibition of the DTH-induced vascular leakage and an increase in serum RMCP II. These findings are consistent with an important role for mucosal mast cells in early vascular leakage changes of intestinal DTH reactions. In addition, sensory nervous control of mucosal mast cell activation early after challenge is demonstrated.

Mast cell activation augments gastric mucosal injury through a leukotriene-dependent mechanism

1994 ◽  
Vol 266 (5) ◽  
pp. G863-G869 ◽  
Author(s):  
K. P. Rioux ◽  
J. L. Wallace
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Receptor Antagonist ◽  
Cell Activation ◽  
Mucosal Injury ◽  
Mast Cell Activation ◽  
Gastric Injury ◽  
Leukotriene D4 ◽  
Mucosal Mast Cells ◽  
Dependent Mechanism

Several lines of evidence suggest a role for mast cells as modulators of gastric mucosal integrity, but the effect of antigenic mast cell activation on mucosal resistance to injury has not previously been examined. In this study, rats were sensitized to the nematode Nippostrongylus brasiliensis and were studied 35-42 days later. With use of an ex vivo gastric chamber preparation, the stomach was exposed for 10 min to 20% ethanol. In some rats, antigen was administered intra-arterially 10 min before application of ethanol. Sensitized rats exhibited similar levels of ethanol-induced gastric injury as control rats, despite having significantly greater numbers of mucosal mast cells. However, antigen administration, which did not in itself produce mucosal injury, significantly augmented (approximately 3-fold) the extent of injury in sensitized but not control rats. Prior treatment with dexamethasone depleted mucosal mast cells in control and sensitized rats. Moreover, this treatment abolished the increase in mucosal injury observed in sensitized rats treated with antigen and topical ethanol. Pretreatment with a leukotriene D4-receptor antagonist, but not a platelet-activating factor-receptor antagonist or a cyclooxygenase inhibitor, abolished the increased susceptibility of sensitized rats to gastric damage induced by antigen and topical ethanol. These results suggest that mucosal mast cell number per se does not influence mucosal susceptibility to injury; however, activation of mast cells markedly increases the susceptibility to injury through a peptidoleukotriene-dependent mechanism.

scholarly journals Impact of Diet on Symptoms of the Irritable Bowel Syndrome

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 575
Author(s):  
Robin Spiller
Keyword(s):  
Mast Cell ◽  
Irritable Bowel Syndrome ◽  
Cell Activation ◽  
Personalised Medicine ◽  
Short Chain Fatty Acids ◽  
Mast Cell Activation ◽  
Bowel Habit ◽  
Gaseous Distension ◽  
Typical Food ◽  
Irritable Bowel

Irritable bowel syndrome (IBS), with its key features of abdominal pain and disturbed bowel habit, is thought by both patients and clinicians to be strongly influenced by diet. However, the complexities of diet have made identifying specific food intolerances difficult. Eating disorders can masquerade as IBS and may need specialist treatment. While typical food allergy is readily distinguished from IBS, the mechanisms of gut-specific adverse reactions to food are only just being defined. These may include gut-specific mast cell activation as well as non-specific activation by stressors and certain foods. Visceral hypersensitivity, in some cases mediated by mast cell activation, plays a key part in making otherwise innocuous gut stimuli painful. Rapidly fermented poorly absorbed carbohydrates produce gaseous distension as well as short-chain fatty acids and lowering of colonic pH which may cause symptoms in IBS patients. Limiting intake of these in low FODMAP and related diets has proven popular and apparently successful in many patients. Existing diet, colonic microbiota and their metabolic products may be helpful in predicting who will respond. Wheat intolerance may reflect the fact that wheat is often a major source of dietary FODMAPs. It may also be either a forme fruste of coeliac disease or non-specific immune activation. Wheat exclusion can be successful in some of these patients. More research is needed to fully understand the mechanisms of food intolerances and how to best ameliorate them in a personalised medicine approach to diet in IBS.

Evidence for Mast Cell Activation in Patients with Therapy-Resistant Irritable Bowel Syndrome

2011 ◽  
Vol 49 (02) ◽  
pp. 191-194 ◽  
Author(s):  
T. Frieling ◽  
K. Meis ◽  
U. Kolck ◽  
J. Homann ◽  
A. Hülsdonk ◽  
...  
Keyword(s):  
Mast Cell ◽  
Irritable Bowel Syndrome ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Irritable Bowel

Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex

2013 ◽  
Vol 305 (5) ◽  
pp. G383-G391 ◽  
Author(s):  
Jacco J. de Haan ◽  
M'hamed Hadfoune ◽  
Tim Lubbers ◽  
Caroline Hodin ◽  
Kaatje Lenaerts ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Mucosal Mast Cell ◽  
Mucosal Mast Cells ◽  
Vagal Reflex ◽  
Anti Inflammatory ◽  
Mouse Mast Cell ◽  
Stimulation Of

Nutritional stimulation of the cholecystokinin-1 receptor (CCK-1R) and nicotinic acetylcholine receptor (nAChR)-mediated vagal reflex was shown to reduce inflammation and preserve intestinal integrity. Mast cells are important early effectors of the innate immune response; therefore modulation of mucosal mast cells is a potential therapeutic target to control the acute inflammatory response in the intestine. The present study investigates intestinal mast cell responsiveness upon nutritional activation of the vagal anti-inflammatory reflex during acute inflammation. Mucosal mast cell degranulation was induced in C57/Bl6 mice by administration of Salmonella enterica LPS. Lipid-rich enteral feeding prior to LPS significantly decreased circulatory levels of mouse mast cell protease at 30 min post-LPS compared with isocaloric low-lipid nutrition or fasting. CCK-1R blockage reversed the inhibitory effects of lipid-rich feeding, whereas stimulation of the peripheral CCK-1R mimicked nutritional mast cell inhibition. The effects of lipid-rich nutrition were negated by nAChR blockers chlorisondamine and α-bungarotoxin and vagal intestinal denervation. Accordingly, release of β-hexosaminidase by MC/9 mast cells following LPS or IgE-ovalbumin complexes was dose dependently inhibited by acetylcholine and nicotine. Application of GSK1345038A, a specific agonist of the nAChR α7, in bone marrow-derived mast cells from nAChR β2−/− and wild types indicated that cholinergic inhibition of mast cells is mediated by the nAChR α7 and is independent of the nAChR β2. Together, the present study reveals mucosal mast cells as a previously unknown target of the nutritional anti-inflammatory vagal reflex.

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