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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies indicated that eosinophils and mast cells accumulate and become activated in inflammatory bowel disorders. The aim of the study was to examine the presence of eosinophil and mast cell mediators in human stool samples of patients with inflammatory bowel disorders. We measured eosinophil cationic protein (ECP), eosinophil protein X (EPX), methylhistamine, and alpha 1-antitrypsin in fecal samples of 136 patients (62 Crohn's disease, 24 ulcerative colitis, 15 intestinal food allergy, 35 other gastrointestinal diseases) and 8 healthy controls. We found strongly elevated levels of ECP (median: 29, range: 0.4-1783 ng/g feces) and EPX (803, 10-33,225 ng/g) in all patients groups compared to controls (ECP: 1.5, 0.5-55 ng/g; EPX: 235, 12-746 ng/g). Similar results, albeit less pronounced, were obtained for methylhistamine and alpha 1-antitrypsin. Particularly high concentrations of ECP and EPX were found in patients with active mucosal inflammation. In conclusion, the study presents an easy and reliable method for the detection of fecal ECP, EPX, and methylhistamine and may provide a tool to gain insight into the pathogenesis of inflammatory bowel diseases and have potential as diagnostic test.
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PMID:Quantification of inflammatory mediators in stool samples of patients with inflammatory bowel disorders and controls. 905 25

Early symptoms of food allergy, including diarrhea, are caused by IgE-mediated anaphylactic reactions. To clarify the mechanisms of IgE-mediated anaphylactic reactions in the intestine induced by orally administered antigen, a mouse model was established by s.c. implantation of a murine hybridoma capable of producing monoclonal anti-trinitrophenyl IgE antibody. Morphologic and immunologic changes in the intestine, as well as the effect of the soluble high affinity IgE receptor alpha chain, were investigated after oral challenge with antigen in this mouse model. Diarrhea, a decrease in s.c. blood flow, an increase in vascular permeability, a substantial increase in serum histamine levels, and noticeable infiltration of mast cells and IgE-bearing cells into the lamina propria were observed around 30 min after antigen challenge. However, these changes were efficiently prevented by pretreatment of the mice with the soluble high affinity IgE receptor alpha chain. These findings suggested that oral administration of antigen actually induced anaphylactic shock in our mouse model. This reaction was most likely to be mediated by mast cell activation, in response to the IgE-antigen complex, and a soluble form of the high-affinity IgE receptor efficiently prevented this IgE-mediated anaphylactic reaction by trapping free IgE.
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PMID:Induction of anaphylaxis in mouse intestine by orally administered antigen and its prevention with soluble high affinity receptor for IgE. 1008 45

There have frequently been doubts as to the relevance of food allergy, in particular as far as the involvement of the intestinal tract is concerned. Several studies, however, have confirmed the existence of allergic reactions in the gut, with an estimated prevalence of about 1-2% in adults. Clinical symptoms are unspecific and include nausea, vomiting, abdominal pain, cramping and diarrhea. Intestinal mast cells, as well as intestinal eosinophils, have been shown to be involved in the pathogenesis of food-allergy-related enteropathy. In addition to classical IgE-dependent degranulation, further agonists have been demonstrated for mast cell activation, for example IL-4. The methods used to confirm the diagnosis of intestinal allergy are still insufficient. Until now, blinded oral challenge procedures with food antigens have been accepted as the 'gold standard' in diagnosing food allergy, although these tests have practical problems. Therefore, new test systems have been developed, such as endoscopic provocation tests, that may improve diagnostic procedures. Elimination diet still presents the main basis of therapy. Aspects to be focused on in the future are the role fo IgE-independent allergic mechanisms in intestinal allergy, the impact of cross-reactivity with other allergens and the relationship to other inflammatory bowel diseases such as Crohn's disease, ulcerative colitis, celiac disease and irritable bowel syndrome.
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PMID:Allergy and the gut. 1082 17

Telangiectasia macularis eruptiva perstans (TMEP) is a rare form of cutaneous mastocytosis observed in less than 1% of cases of mastocytosis. Clinically, anaphylaxis may appear as a result of increased mast cell degranulation in different circumstances. A case of TMEP presented as pseudoallergic reactions to foods is reported in which the appearance of typical lesions on the trunk and their histological analysis together with a negative food allergy study confirmed the diagnosis.
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PMID:Telangiectasia macularis eruptiva perstans presented as a pseudoallergic food reaction. 1103 43

1. This in vitro study was designed to determine the potential use of the NK(1) antagonist, SR140333 as an anti-diarrhoeal treatment for food allergy or inflammatory bowel disease. The effect of various immune and neuronal stimuli on human colonic substance P (SP) release and the effect of SR140333 on subsequently stimulated mucosal ion transport was investigated. 2. Submucosal and sensory nerve fibre stimulation using electrical field stimulation (1 ms/7 Hz/7 V) and capsaicin (50 microM) respectively, mast cell activation by anti-IgE (1/250 dilution) and granulocyte stimulation using fMLP (50 microM) each released SP and evoked a secretory response. 3. SP and the NK(1) selective agonist, Sar-SP (0.1 - 1000 nM) stimulated an increase in colonic secretion which was antagonized by SR140333 (pD'(2)=6.7 and 7.25 versus SP and Sar-SP respectively). 4. SR140333, at a concentration that blocked NK(1)-mediated secretion (500 nM), also reduced the secretory response to both alphaIgE and capsaicin. This suggests a pathophysiologic role for NK(1) receptors. 5. Capsaicin evoked SP release was increased in tissue taken from Crohn's disease but not ulcerative colitis patients. The response to SP was however reduced by 70 and 89% respectively. 6. Mast cells and sensory afferents contribute to allergic diarrhoea. Since SR140333 reduced the secretory response to mast cell and afferent stimulation this compound may be particularly useful in reducing the symptoms of food allergy.
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PMID:Human colonic anti-secretory activity of the potent NK(1) antagonist, SR140333: assessment of potential anti-diarrhoeal activity in food allergy and inflammatory bowel disease. 1149 21

There are no evidence-based studies of the treatment of patients with eosinophilic gastroenteritis. Treatment decisions depend on experience gained from observations linking causative entities, principal clinical manifestations, and anticipated natural history of the disease. Because clinical symptoms and organ involvement probably vary with etiology, classification as to the likely cause (eg, food allergy or other dietary intolerance, idiosyncratic drug reaction, occult infection, idiopathic) determines the decisions made about dietary, pharmacologic, and surgical treatment. Elimination of foods and the use of elemental diets, corticosteroids, and mast cell inhibitors (eg, cromolyn sodium, ketotifen), alone or in combination, all have their place, depending on the age of the patient, organ involved, clinical presentation, and clinical urgency. Isolated cases are diagnosed only at surgical exploration for acute abdominal catastrophes; in these instances, further therapy depends on whether resection is done, but most patients remain in remission after surgery. Occult parasitism remains an elusive and unrecognized cause of an unknown number of cases, suggesting that empiric antihelminthic therapy should be tried in some patients. Individual reports of success with nonsystemic steroids and leukotriene inhibitors have been published.
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PMID:Eosinophilic Gastroenteritis. 1179 33

Urticaria and angioedema evoke a completely different differential diagnosis from angioedema without an associated urticarial syndrome. This review of the literature is to give the reader a global insight into the spectrum of urticaria and angioedema, focusing on differential diagnosis and pathogenic mechanisms. It will define the role of the mast cell, explore a possible autoimmune basis for urticaria, and examine the purported role of food allergy in chronic urticaria. Last, the work-up and treatment will be discussed. Urticaria and angioedema are frustrating problems for both physicians and their patients; however, the problem can best be approached by considering urticaria as a symptom rather than a specific disease. The physical examination and medical history remain the two most important pieces of information.
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PMID:Urticaria and angioedema. 1247 45

The purpose of this review, based on studies from our laboratory as well as from others, is to summarize salient features of mast cell immunobiology and to describe their associations with gastrointestinal mucosal defense. Gastrointestinal mast cells are involved in many pathologic effects, such as food hypersensitivity. On the other hand, they also play a protective role in defense against parasitic and microbial infections. Thus, they have both positive and negative effects, but presently the mechanisms that control the balance of these various effects are poorly known. It has been suggested that stabilization of mast cells may be a key mechanism to protect the gastrointestinal tract from injury. Few molecules are known to possess both mast cell stabilizing and gastrointestinal cytoprotective activity. These include zinc compounds, sodium cromoglycate, FPL 52694, ketotifen, aloe vera, certain flavonoids such as quercetin, some sulfated proteoglycans such as chondroitin sulfate and dehydroleucodine. Dehydroleucodine, a sesquiterpene lactone isolated from Artemisia douglasiana Besser, exhibits anti-inflammatory and gastrointestinal cytoprotective action. The lactone stimulates mucus production, and inhibits histamine and serotonin release from intestinal mast cells. The lactone could act as a selective mast cell stabilizer by releasing cytoprotective factors and inhibiting pro-inflammatory mast cell mediators.
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PMID:Role of mast cells in gastrointestinal mucosal defense. 1451 Feb 34

Although food allergy has emerged as a major health problem, the mechanisms that are decisive in the development of sensitization to dietary Ag remain largely unknown. CTLA-4 signaling negatively regulates immune activation, and may play a crucial role in preventing induction and/or progression of sensitization to food Ag. To elucidate the role of CTLA-4 signaling in responses to food allergens, a murine model of peanut allergy was used. During oral exposure to peanut protein extract (PPE) together with the mucosal adjuvant cholera toxin (CT), which induces peanut allergy, CTLA-4 ligation was prevented using a CTLA-4 mAb. Additionally, the effect of inhibition of the CTLA-4 pathway on oral exposure to PPE in the absence of CT, which leads to unresponsiveness to peanut Ag, was explored. During sensitization, anti-CTLA-4 treatment considerably enhanced IgE responses to PPE and the peanut allergens, Ara h 1, Ara h 3, and Ara h 6, resulting in elevated mast cell degranulation upon an oral challenge. Remarkably, antagonizing CTLA-4 during exposure to PPE in the absence of CT resulted in significant induction of Th2 cytokines and an elevation in total serum IgE levels, but failed to induce allergen-specific IgE responses and mast cell degranulation upon a PPE challenge. These results indicate that CTLA-4 signaling is not the crucial factor in preventing sensitization to food allergens, but plays a pivotal role in regulating the intensity of a food allergic sensitization response. Furthermore, these data indicate that a profoundly Th2-biased cytokine environment is insufficient to induce allergic responses against dietary Ag.
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PMID:CTLA-4 signaling regulates the intensity of hypersensitivity responses to food antigens, but is not decisive in the induction of sensitization. 1561 Dec 39

This study investigated whether orally administered probiotic bacteria (Bifidobacterium bifidum and Lactobacillus casei) and a gram-negative bacterium (Escherichia coli) function as allergic immune modulators to prevent food allergy, according to the hygiene hypothesis. C3H/HeJ mice were sensitized with ovalbumin (OVA) and cholera toxin for 5 weeks. After sensitization, the OVA-induced mice that were not treated with bacteria had significantly increased levels of OVA-specific IgE, total IgE, and IgG1 in sera, as well as scab-covered tails. In comparison, groups treated with B. bifidum BGN4 (BGN4), L. casei 911 (L. casei), or Escherichia coli MC4100 (E. coli) had decreased levels of OVA-specific IgE, total IgE, and IgG1, and decreased levels of mast cell degranulation and tail scabs. OVA-specific IgA levels were decreased in BGN4- and L. casei-treated groups. In conclusion, administration of E. coli, BGN4, or L. casei decreased the OVA-induced allergy response. However, a normal increase in body weight was inhibited in the E. coli-treated mice and in the montreated mice groups during allergy sensitization. Thus, BGN4 and L. casei appear to be useful probiotic bacteria for the prevention of allergy.
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PMID:Oral probiotic bacterial administration suppressed allergic responses in an ovalbumin-induced allergy mouse model. 1596 6


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