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

Mastocytosis is characterized by increased proliferation of mast cells. Two patients had systemic mastocytosis involving the skin and gastrointestinal tract, complicated by malabsorption and tetany. Absorption studies in these patients suggested that the entire small bowel was involved and that the defect was mild in the absence of diarrhea. Small bowel biopsies disclosed infiltration of the lamina propria and submucosa by mast cells, and gastrointestinal tract x-ray films showed nodular densities, edema, and thickening of the bowel wall. Tetany was due in part to combined hypocalcemia, hypomagnesemia, and hypokalemia. Diarrhea and malabsorption were due to mast cell infiltration of the bowel rather than to histamine. patients with signs of systemic mastocytosis should have careful evaluations and be followed up to prevent development of malabsorption and tetany.
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PMID:Tetany, malabsorption, and mastocytosis. 119 Sep 35

Excessive fluid and electrolyte secretion, resulting symptomatically in diarrhea, has been associated with mast cell activation in a variety of experimental and clinical settings. The present study has used a human colonic epithelial cell line to examine mechanisms underlying this phenomenon. Acute addition of mixed mast cell mediators (as a lysate of rat basophilic leukemia cells) to epithelial cells led to prompt and sustained chloride secretion. The response was partially inhibitable by an antihistaminic drug and an adenosine antagonist, suggesting that histamine, adenosine, and possibly other mediators are responsible for producing the acute effect. Supernatants from immunologically activated rat basophilic leukemia cells had similar effects. Chronic exposure of epithelial cells to the lysate mediator preparation, followed by washing, had no effect on their basal electrical or electrolyte-transporting properties. However, the chloride secretory response of the cells to subsequent addition of vasoactive intestinal peptide, carbachol, and heat-stable enterotoxin of Escherichia coli was significantly enhanced, whereas responses to an adenosine agonist or PGE1 were unaffected. This study has, therefore, demonstrated two ways in which mast cell mediators can directly influence intestinal epithelial cells to secrete more chloride and, hence, to enhance fluid secretion in the gut. The findings may be of relevance to our understanding of inflammatory diarrhea and may aid the development of novel therapies for this disorder.
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PMID:Immune-related intestinal chloride secretion. III. Acute and chronic effects of mast cell mediators on chloride secretion by a human colonic epithelial cell line. 165 Mar 88

This article reports on a 53-year-old woman suffering from recurrent diarrhea since 1980 who, in November 1988, was admitted to the Medical Department of the University of Erlangen-Nuremberg with four to eight loose to liquid stools a day. Since January 1988, in addition to abdominal symptoms, including meteorism and recurrent abdominal pain, intermittent bouts of fever of up to 40 degrees C lasting six to eight hours and frequently occurring in the evening, had been noted. The patient's symptoms improved at weekends and during the holidays. Since 1977, she had been employed at a cheese counter, selling cheese. Noteworthy findings were an eosinophilia of 6% and, with the prick skin test, weakly positive reactions induced by two moulds with no increased total IgE and negative IgE RAST for diverse foods and moulds. An in vitro histamine-releasing test performed on colonic mucosal particles obtained at colonoscopy, a sensitization of the mucosa to moulds was demonstrated, and the patient was then given the mast cell stabilizing agent DNCG. This treatment cleared the symptoms, and she put on weight. In vitro tests on colonic biopsy material repeated in 1989 revealed a significant reduction in the release of histamine in response to the anti-allergic treatment.
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PMID:[Allergic enteropathy. Intestinally-mediated fungus allergy]. 172 12

Deliberately spoiled mackerel samples and mackerel samples implicated in outbreaks of scombrotoxicosis were, under medical supervision, tested blind on normal, healthy volunteers of both sexes. These experiments identified batches of fish which could induce nausea/vomiting and/or diarrhoea when 50 g samples were consumed. It was also established that the fillets in a batch were neither of equal potency nor homogeneous with respect to histamine content. Strong evidence was obtained that dietary histamine is not a major determinant of scombrotoxicosis since potency was not positively correlated with the dose, and volunteers appeared to fall into susceptible and non-susceptible subgroups. However, there is no reason to suspect allergy as being solely responsible for these differences in sensitivity. It is also possible to discount body weight as a factor. While the data suggest that females may be more susceptible than males, this effect cannot be confirmed at the present time. Studies with susceptible volunteers predosed with either placebo or H1 antagonist (chlorpheniramine 4 mg) demonstrated convincingly that the antihistamine can abolish vomiting and diarrhoea associated with the ingestion of 50 g of scombrotoxic fish. It is therefore postulated that endogenous histamine released by mast cell degranulation has a significant role in the aetiology of scombrotoxicosis, whereas the role of dietary histamine is minor. The nature and origin of the agent responsible for mast cell degranulation is being investigated.
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PMID:The importance of endogenous histamine relative to dietary histamine in the aetiology of scombrotoxicosis. 180 4

The in vitro histamine release response of human intestinal mast cells and basophils challenged with anti-IgE, Concanavalin A, ionophore A23187 and food extracts was compared with skin prick test, RAST analysis and open food challenge. It was not possible to perform food challenge in all patients; however, seven children underwent open food challenge and in five the clinical diagnosis of "true" food allergy was confirmed. The intestinal mast cells were pooled from enzymatically dispersed duodenal biopsies obtained by duodenoscopy from 15 selected children suspected of food allergy, and five age-matched controls. In nine of 10 patients classified as "food allergic" intestinal mast cells released histamine to various food extracts in a dose-dependent fashion. From the mast cells of the nine food-allergic patients compared with non-allergics, the anti-IgE mediated mast cell histamine release was increased. Additionally, at 1000 U/ml anti-IgE the mast cell histamine release was increased compared with their corresponding basophils. However, in non-allergic subjects the histamine release of basophils was increased compared with their corresponding mast cells. Histamine release from basophils was positively correlated to the test scores of the RAST analysis, skin prick test, and food challenge. No apparent correlation between tests scores obtained from histamine release of intestinal mast cell and the other tests was demonstrated, except in children with diarrhoea as only symptom. However, the study gives evidence that duodenal mast cells actually are sensitized with specific IgE and thus may play a pathophysiological role in food hypersensitivity. In addition, the study shows that the ability of different stimuli, including food extracts, to trigger basophil histamine release does not correlate with their potency to induce histamine release from mast cells.
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PMID:Comparison of intestinal mast cell and basophil histamine release in children with food allergic reactions. 248 85

The intracerebroventricular (ICV) injection of the mast cell degranulator Compound 48/80 (2.5-2.0 micrograms/kg) produced a marked behavioral syndrome in normotensive rats. The behaviors included head and body shakes, paw tremor, excessive grooming, unusual posture and gait, mild diarrhoea, piloerection, extreme agitation and irritability to touch, and a later phase of sedation. The highest doses (15 and 20 micrograms/kg) also produced catalepsy and episodes of "barrel rolling" (continuous rolling of 1-8 turns around the longitudinal axis). These behaviors were observed for approximately 15-30 min although the sedation and catalepsy were maintained for 90-120 min. A second ICV injection of the 10 micrograms/kg dose of Compound 48/80 given 2 hr after an initial injection of this dose, produced a much reduced response and the numbers of head and body shakes, and episodes of paw tremor and grooming were between 20-30% of those produced by the first injection. The reduced effect of the second injection indicates that the behavioral effects of Compound 48/80 may arise from the acute degranulation of mast cells rather than direct effects on neuronal populations or the cerebral vasculature.
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PMID:Acute intracerebroventricular injections of the mast cell degranulator compound 48/80 and behavior in rats. 278 Jul 92

Twenty-one patients were entered into a phase I trial to evaluate toxicity, antitumor effects, and biological responses at tumor sites during treatment of R24, an immunoglobulin G3 (IgG3) mouse monoclonal antibody (mAb) against GD3 ganglioside. Toxicity was related to dose of R24. Urticaria and pruritus were the most prominent side effects, with nausea, vomiting, and diarrhea occurring at the highest dose levels. Partial responses were observed in four patients lasting from 6 to 46 weeks, and mixed responses were seen in two patients. Responses occurred as early as 4 weeks and as late as 10 weeks after beginning treatment. Twenty of the 21 patients developed human IgG antibodies against R24. Antimouse Ig antibodies were first detected at a median of 14 days after starting treatment, but three of the four patients who had a partial response developed the antimouse Ig responses later than 20 days. Peak serum levels of R24 were related to dose and ranged from a mean of 0.9 micrograms/mL at the lowest dose level (1 mg/m2/d) to 44 micrograms/mL at the highest dose (50 mg/m2/d). The amount of R24 reaching tumor sites corresponded to the dose administered, and R24 could be detected in tumors as late as 30 days after finishing treatment. Inflammation at tumor sites was observed during treatment. Biopsies of tumors taken before, during, and after treatment revealed that R24 induced deposition of complement components, increased numbers of mast cells with mast cell degranulation, and infiltration of T lymphocytes. These results suggest that treatment with R24 can produce a localized inflammatory response at tumor sites that is capable of producing tumor regression.
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PMID:Phase I trial of a mouse monoclonal antibody against GD3 ganglioside in patients with melanoma: induction of inflammatory responses at tumor sites. 317 29

The clinical and pathologic features of systemic mastocytosis in 16 dogs are reported. There was no apparent breed or sex predilection, and the median age at presentation was 9.5 years. In 14 of 16 cases there was a primary cutaneous mast cell tumor (MCT). When cutaneous tumor location was compared with previous reports, there was no association between location and systemic dissemination. The most common presenting signs associated with the cutaneous tumor were regional dissemination, edema, ulceration, and abscessation. They were present in 12 dogs (69%). Signs of systemic illness, including anorexia, vomiting, and diarrhea, were seen in eight dogs (50%). Other than the cutaneous tumors, the most consistent physical and radiographic abnormalities included lymphadenopathy, splenomegaly, and hepatomegaly. Eosinophilia and basophilia were seen in two and five dogs, respectively. Six dogs had increased numbers of mast cells in peripheral blood or buffy coat smears. Five of the nine dogs evaluated had increased numbers of mast cells in bone marrow aspirates. Bone marrow aspiration was superior to both peripheral blood and buffy coat smears in predicting mastocytosis. Coagulation abnormalities were seen in three of five dogs tested. Using a conventional histomorphologic grading system, 10 of 13 (77%) tumors were classified as Grade III or undifferentiated and were overrepresented when compared with previous reports of cutaneous MCTs. Eighty-eight percent of the dogs either died or were euthanatized because of their tumors. Organs commonly involved at necropsy included lymph nodes, spleen, liver, and bone marrow; four dogs had gastroduodenal ulcers.
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PMID:Systemic mastocytosis in 16 dogs. 350 91

The intracerebroventricular injection of the mast cell degranulator, compound 48/80 (C48/80, 10 micrograms/kg), produced a marked behavioural syndrome in rats which included head and body shakes, paw tremor, excessive grooming, unusual posture and gait, mild diarrhoea, piloerection, extreme agitation and irritability to touch, sedation and catatonia. Fifteen minutes after C48/80, the histamine concentrations were decreased significantly in all brain regions examined, i.e. the cortex, cerebellum, midbrain, medulla oblongata-pons (MO-P) and hypothalamus. The noradrenaline (NA) concentrations were decreased in the cerebellum, hypothalamus and MO-P, whereas the dopamine (DA) content was decreased in the MO-P only. The concentrations of serotonin were not affected. As such, the behaviours following the acute degranulation of brain mast cells by C48/80 may result predominantly from the release of histamine and possibly NA and DA.
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PMID:The effects of intracerebroventricular administration of compound 48/80 on behaviour and regional brain amine concentrations in the rat. 370 80

Thirteen patients with systemic mast cell disease were studied in order to define the hepatic changes in this disease and to correlate the histologic lesions in the liver with the clinical findings. These patients often presented with multisystem disorders and 10 had hepatomegaly. Microscopically, the liver tissues in all patients showed fibrosis and chronic inflammatory cellular infiltration with plasma cells, lymphocytes, eosinophils, and mononuclear fibroblast-like cells in the portal area. The hepatic sinusoids were not significantly involved. A histologic diagnosis of systemic mast cell disease is seldom entertained in liver biopsy specimens embedded in paraffin and stained with hematoxylineosin, but can be facilitated in biopsy specimens embedded in plastic such as methacrylate. Tissue mast cells in the cellular infiltrate can be demonstrated best by special staining techniques with Giemsa, toluidine blue, and chloroacetate esterase. The severity of the histologic changes in the liver does not correlate well with the size of the liver or biochemical changes in the blood. Abnormal serum biochemical values were noted primarily in those with dehydration caused by diarrhea and vomiting, and in those with malnutrition. Hepatic function test results were usually normal, except for alkaline phosphatase level, which was elevated in all 13 patients. Although the clinical significance of hepatic involvement in systemic mast cell disease cannot be established with certainty in this study, it is believed that the prognosis of systemic mast cell disease is most intricately related to the systemic effects of mast cell involvement in many other organs, and not to hepatic involvement per se.
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PMID:Hepatic involvement in systemic mast cell disease. 370 70


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