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

Lymph nodes from 21 cases of generalized mastocytosis were studied histologically to confirm or exclude mast cell infiltration, and to investigate their micro-architecture. Mast cell infiltrates were detected in 17 (80%) of the lymph nodes and were found mainly in the medullary cords and sinuses. Diffuse infiltration was seen in 14 cases and focal infiltration in three cases. The following pathological findings were frequently observed: germinal centre hyperplasia (n = 14), which is probably a nonspecific finding; and hyperplasia of small blood vessels, which sometimes resembled high endothelial venules (14), eosinophilia (8), plasmacytosis (7) and collagen fibrosis (6), all of which may well be related to the effects of mediators released by mast cells. Infiltrates of acute or chronic myeloid leukaemia were seen in six lymph nodes. Division of the cases into two prognostically different groups, i.e. systemic mastocytosis, in which the skin lesions of urticaria pigmentosa are present and the prognosis is favourable, and malignant mastocytosis, in which there is no cutaneous involvement and the prognosis is poor, revealed that all six lymph nodes exhibiting leukaemic infiltrates came from the malignant mastocytosis group; eosinophilia, plasmacytosis and fibrosis were seen significantly more often in malignant than in systemic mastocytosis, but blood vessel hyperplasia and germinal centre hyperplasia were encountered with the same high frequency in both groups; and mast cell atypia tended to be more pronounced in malignant mastocytosis; this diagnosis could therefore easily be missed without naphthol AS-D chloroacetate esterase staining.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymph node findings in generalized mastocytosis. 145 27

Comparative studies were made of two populations of Sprague-Dawley rats infected with Hymenolepis diminuta. The time course of infection, the development of mucosal mastocytosis and the levels of rat mucosal mast cell (MMC) protease (RMCP II) in serum and in jejunal mucosal tissues were monitored at intervals after infection with 40 cysticercoids of the tapeworm. Worm expulsion patterns differed markedly between the two populations, rats of New Zealand origin showing an abrupt and clear-cut loss of worms, rats of English origin showing a more gradual decline over a longer time period. In both populations, however, numbers of MMC and levels of tissue RMCP II were positively correlated with time after infection and negatively correlated with worm numbers. In only one of the three experiments (using English strain rats over a short time period) did levels of serum RMCP II change with time. In the other two experiments, in which English-strain and New Zealand-strain rats were used, there were no correlations between serum RMCP II and time, numbers of MMC, numbers of worms or levels of tissue RMCP II. The absence of correlation between serum RMCP II and worm loss in these experiments implies that MMC have no direct role in expulsion of H. diminuta. The data do show, nevertheless, that this purely luminal tapeworm is fully capable of activating the mucosal T lymphocyte-MMC precursor axis to elicit a mucosal mastocytosis.
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PMID:Inflammatory responses in the intestine during tapeworm infections. Mucosal mast cells and mucosal mast cell proteases in Sprague-Dawley rats infected with Hymenolepis diminuta. 145 91

Generalised mastocytosis is a rare condition characterised by the clinical features of the release of vasoactive peptides from tissue mast cells infiltrating in the reticuloendothelial tissues. The mast cell however appears to have its origin in the pluripotential bone marrow stem cell committed to a basophil and it is therefore not surprising that myeloproliferative and myelodysplastic disorders commonly co-exist or terminate the clinical phase of mastocytosis. Both abnormal proliferation and maturation of the myeloid committed cells are found. Non-Hodgkin's lymphoma can occur before and after mastocytosis becomes manifest. While this is statistically a random event the relationship between lymphokines and mast cell differentiation and proliferation raises the possibility of a benign reactive lymphoid event eventually becoming malignant.
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PMID:Mastocytosis and co-existent non-Hodgkin's lymphoma and myeloproliferative disorders. 147 31

The mast cell, equipped with enzymes, chemotactic factors, a vasoactive amine, an anticoagulant, and lipid-derived proinflammatory products, may be essential in tissue modeling as well as in defense. Its primarily perivascular location in skin and the mucosa of the respiratory tract and the gut assures its availability to counter parasites. By the same token, the mast cell is responsible for interactions with inhaled, ingested, and injected antigens that comprise IgE-mediated allergic reactions. Abnormally high numbers of mast cells in the skin, either localized or generalized, result in urticaria pigmentosa or generalized cutaneous mastocytosis, respectively. Tissue infiltration by excessive mast cells, primarily in gut, bone, liver, and spleen, results in systemic mastocytosis; this may be accompanied by myelodysplasia or lymphoma and may eventuate in mast cell leukemia. Until the etiology of mastocytosis is understood, the treatment is symptomatic: histamine antagonism by H1 +/- H2 blockade for flushing, itching, and gastric distress; cyclooxygenase inhibition to prevent prostaglandin D2 (PGD2)-induced hypotension when indicated; and oral cromolyn to prevent gastrointestinal symptoms and bone pain.
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PMID:Mast cell disease. 149 Jun 22

Topical application of capsaicin to the gastric mucosa results in marked hyperemia as a consequence of the release of vasoactive neuropeptides from sensory afferent neurons. Because many of these neuropeptides have the capacity to induce mast cell degranulation, we investigated the possible contribution of mast cells to capsaicin-induced hyperemia. Application of capsaicin to the gastric mucosa of normal rats resulted in a concentration-dependent increase in blood flow. In rats in which mastocytosis was induced by prior infection with Nippostrongylus brasiliensis, the hyperemic responses to capsaicin were significantly greater than in control rats. This augmented hyperemic response could be significantly attenuated by pretreatment with a histamine H1-receptor antagonist (pyrilamine) or with a mast cell stabilizer (doxantrazole). Depletion of mucosal mast cells through treatment with dexamethasone also significantly reduced the hyperemic response to capsaicin. Hyperemic response to capsaicin in normal rats and in rats with mucosal mastocytosis could be completely abolished by pretreatment with ruthenium red or prior ablation of the sensory afferent neurons with capsaicin. These results suggest that in rats with gastric mastocytosis, sensory neuron-dependent activation of mast cells contributes to the hyperemic response to topical capsaicin. These findings are therefore consistent with the hypothesis that there is communication between nerves and mast cells in the gastric mucosa, at least in rats previously infected with N. brasiliensis.
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PMID:Capsaicin-induced hyperemia in the stomach: possible contribution of mast cells. 151 32

Erythrodermic mastocytosis is a rare variant of diffuse cutaneous mastocytosis in which the skin becomes red, thickened, and lichenified and has a doughy consistency with multiple small papules on its surface, giving a leathery appearance to the skin. In this report, I describe a curious case of erythrodermic mastocytosis that appears to be due to vasodilation rather than to mast cell infiltration of the skin. In my opinion, this case might be an example of generalized telangiectasia macularis eruptiva perstans. Results of all laboratory tests failed to demonstrate systemic mast cell involvement; therapy with a combination of H1 and H2 antihistamines plus disodium cromoglycate controlled the symptoms.
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PMID:Erythrodermic mastocytosis. 153 60

The factor(s) that causes excessive mast cell (MC) proliferation in indolent forms of mastocytosis is not known, nor is it known whether that proliferation is a regulated clonal expansion or merely a non-neoplastic hyperplasia. Human MCs display phenotypes that depend on the microenvironment. Thus, if the phenotype of MCs in mastocytosis lesions is determined to be abnormal for that tissue site (and therefore the MCs are refractory to microenvironmental signals) then a clonal process would be suggested. The authors determined the phenotypes of MCs from the lesional skin of 17 patients with indolent mastocytosis and the bone marrows of 9 patients. They compared them with the phenotypes of MCs from the lesional skin of 8 patients with various dermatitides, the skin of 2 patients with idiopathic anaphylaxis, and the breast skin of 15 control patients. MCs from all the skin specimens showed the characteristic skin MC phenotype, with predominantly scroll-poor granules by ultrastructure and containing tryptase and chymase by immunofluorescence detection (the MCTC immunophenotype). The skin MCs of each patient bound avidin and contained carboxypeptidase by immunofluorescence detection. MCs from the bone marrow of patients with indolent mastocytosis, the source of progenitors, also showed the scroll-poor and MCTC phenotypes. These findings do not support an unregulated clonal expansion in indolent forms of mastocytosis. They are consistent with a non-neoplastic hyperplasia or possibly a clonal process in which MCs remain responsive to microenvironmental regulation.
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PMID:Mast-cell phenotype in indolent forms of mastocytosis. Ultrastructural features, fluorescence detection of avidin binding, and immunofluorescent determination of chymase, tryptase, and carboxypeptidase. 156 49

Thirty two cases of the association of mastocytosis and bone lesions were collected in a multicentre study. Five cases involved osteocondensation forms. However, most often (27 cases), there was osteoporosis (OP). The diagnosis was made in the absence of obvious risk factors, and thus often in men (2/3 of patients), when there was the association of pigmented urticaria and an excess of mast cells in bone biopsies. Laboratory, radiological and isotope scan findings are often non-specific, being identical to those encountered in common OP. The histomorphometric profile involves an association of decreased cancellous bone volume, increased area of resorption and decreased bone formation parameters. Progression to malignant mastocytosis occurs essentially in diffuse osteocondensation forms and is rare in OP types. Emphasis must be placed on the importance of qualitative study of bone marrow, using specific stains, since the diagnosis may be missed in the absence of typical skin lesions. Conversely, since a simple increase in mast cell count is possible during common OP, a search for mast cell nodules is important in order to establish the diagnosis with certitude.
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PMID:[Mastocytosis and bone manifestations. Results of the survey of the bone and phosphorus-calcium metabolism section of the French Society of Rheumatology]. 157 47

Bone mastocytosis is characterized radiographically in some patients by diffuse osteosclerosis and in others by demineralization. The reason for these apparently conflicting bone features is unknown. Bone remodeling and marrow mastocytosis infiltration were studied in nine cases of mastocytosis with bone marrow involvement. Six men, ranging from 42 to 78 years of age, and three women, 43, 55, and 73 years old, comprised the series. Two patients had severe and diffuse osteosclerosis. Seven had diffuse demineralization, with crushed vertebrae in four, suggesting common osteoporosis. In three of the seven, cutaneous mastocytosis was absent. Bone biopsies were undecalcified and stained with toluidine blue. In the seven patients with demineralization, the number of marrow mastocytes was increased (154 +/- 24 versus 2 +/- 0.5/mm2 in normal postmenopausal osteoporosis). Mastocyte nodules covering 1-9% of the marrow area were present in all seven patients. These patients showed a significant increase in remodeling; bone formation rate was increased, coupled with a decrease in mean wall thickness. Concomitantly, osteoclast surfaces were increased, with an increased amount of bone resorbed. The two patients with diffuse osteosclerosis had a markedly different histology; mast cell infiltration was dramatically increased (mastocyte count greater than 1000/mm2) with diffuse marrow fibrosis. Bone volume was increased as well, and most of the bone was woven with an intratrabecular mineralization defect. High bone remodeling and decreased osteoblast activity can explain bone loss in mastocytosis with demineralization. Mastocytosis with osteosclerosis is characterized by a more extensive marrow mast-cell infiltration and fibrosis.
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PMID:Bone mastocytosis. A report of nine cases with a bone histomorphometric study. 160 Jun 67

Infection of rats with the parasite Nippostrongylus brasiliensis results in severe intestinal pathology and dysfunction. Much of the damage that occurs within the intestinal tract may be the direct result of the production of potent inflammatory mediators. PAF is one such lipid mediator that may lead to the altered motility and secretory changes that occur during N. brasiliensis infection. Male, Sprague-Dawley rats were subcutaneously infected with 3000 third stage larvae, while control groups were injected with phosphate buffered saline. At various times post infection (4-42 days) groups of four or more infected and control rats were killed and samples of ileum and jejunum were removed for determination of PAF and leukotriene synthesis (LTB4 and LTC4), myeloperoxidase (MPO) activity and tissue eosinophil and mast cell numbers. Separate groups of rats were killed at similar times for the determination of intestinal worm burden and serum rat mast cell protease II (RMCP-II) levels. Significant elevation in PAF synthesis was not seen until day 15, a time when the intestinal worm burden was no longer evident. Furthermore, this elevation was restricted to the jejunum. The elevation in PAF synthesis correlated with a significant elevation in histologically detectable eosinophils and mast cells in the jejunum. Mast cell activity, as detected through serum concentrations of RMCP-II, was significantly elevated at day 8 post-infection and remained elevated until day 18 post-infection. However, despite significant changes in ileal eosinophil and mast cell numbers, PAF synthesis in the ileum did not differ significantly over the course of the infection. LTB4 and LTC4 production and MPO activity, were significantly elevated in both ileum and jejunum only following worm loss. These results demonstrate that PAF synthesis is altered following primary infection with N. brasiliensis. Changes in PAF synthesis paralleled changes in synthesis of other inflammatory mediators and were associated with hyperplasia of various inflammatory cells. Nevertheless, elevated PAF production is not simply a consequence of intestinal eosinophil and mast cell hyperplasia, as ileal PAF production did not significantly change despite hyperplasia of these cell types.
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PMID:Intestinal platelet-activating factor synthesis during Nippostrongylus brasiliensis infection in the rat. 165 65


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