Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article describes the etiology, clinical signs, diagnosis, and treatment of various equine nodular diseases. Although of different etiologies, this group of diseases shares a common histologic reaction pattern characterized by infiltration of eosinophils and collagen degeneration. Collagenolytic granuloma, axillary nodular necrosis, unilateral papular dermatosis/eosinophilic folliculitis, amyloidosis, habronemiasis, and mast cell tumors are discussed.
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PMID:Eosinophilic nodular dermatoses. 763 67

Skin mast cells have been proposed to be involved in the pathogenesis of acute and chronic phases of atopic dermatitis (AD). The aim of the present study was to investigate the significance of different mast cell mediators during acute exacerbation of this frequent skin disease. Plasma levels from 19 patients with AD were screened for elevation of the mast cell-specific protease tryptase, the biogene amine histamine, and the arachidonic acid metabolite prostaglandin D2. None of the patients showed elevated plasma levels of these three mediators, whereas the mean serum IgE level was strongly elevated. We conclude that the investigated mediators are either only active on the cutaneous level or that other mediators are responsible for the development of the acute eczematous and pruritic skin reactions. Alternatively, the assays could have been insufficiently sensitive since some studies have demonstrated increased plasma histamine levels, e.g. after food challenge of such patients.
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PMID:Investigations on plasma levels of mast cell mediators in acute atopic dermatitis. 819 85

This study reports on the usefulness of skin mast cell quantification (mast cells(mm2) as a parameter for the diagnosis of atopic dermatitis (AD) and for determining the efficacy of the therapeutic measures employed. Fifteen children with AD of moderate to extreme severity, and which started within the first two years of life, were studied. The therapeutic measures were limited to advice regarding the choice of adequate living conditions and of an appropriate diet in conjunction with the oral administration of hydroxyzine. Before treatment, 11 children with active AD were submitted to biopsies of both affected and non-affected skin. After treatment, in six children who were asymptomatic for at least one month, another biopsy was performed at a site of previous skin disease. A biopsy of a previously affected site was also performed in the other four children with a personal history of AD and who had no symptoms for more than one year. Treatment with hydroxyzine significantly reduced the number of papillar and reticular mast cells/mm3 of affected skin. In children who had been asymptomatic for one month, the number of papillar dermis mast cells/mm3 was greater than in those who had been asymptomatic for 12 months. In both groups of asymptomatic children, the number of mast cells/mm3 of affected skin was greater than in non-affected skin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mast cell quantification in the skin of children with atopic dermatitis: its value in diagnosis and in assessing the effectiveness of therapy. 855 90

Chronic proliferative dermatitis is a spontaneous mutation in C57BL/Ka mice (cpdm/cpdm), showing alopecia, epithelial hyperproliferation, infiltration by eosinophils and macrophages, and vascular dilatation. To further elucidate its pathogenesis, organs of 1-, 2-, 3-, 4-, 5-, and 6-week-old cpdm/cpdm mice were examined. At 4 weeks, the epidermal thickness was increased, whereas already at 3 weeks, the bromodeoxyuridine incorporation was increased in the basal keratinocytes. However, already at the age of 1 week, skin, lungs, and lymph nodes were infiltrated by eosinophils although no macroscopic lesions were present. Compared with control animals, 6-week-old cpdm/cpdm mice had decreased serum IgE levels and increased numbers of mast cells. From the age of 1 week these mast cells became increasingly IgE positive. In contrast, the mast cells of the control animals remained IgE negative. Mast cells of control and cpdm/cpdm mice were interleukin-4 and tumor necrosis factor-alpha positive. A likely explanation for the tissue infiltration of eosinophils could be the release of interleukin-4 and tumor necrosis factor-alpha from activated mast cells. Tumor necrosis factor-alpha may lead to the expression of E-selectin on endothelial cells, facilitating interleukin-4-mediated eosinophil transendothelial migration. Although various pathogenetic aspects of the cpdm/cpdm mouse need further elucidation, this model can be a tool to study eosinophil infiltration, leukocyte-endothelial cell interactions, and mast cell proliferation. Furthermore, the cpdm/cpdm mouse can be used to study chronic inflammatory skin disease because of the severe epidermal proliferation.
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PMID:Pathogenesis of skin lesions in mice with chronic proliferative dermatitis (cpdm/cpdm). 877 48

A case of spontaneous occurrence of systemic mast cell disease in a non-treated laboratory-reared gerbil is reported. This case corresponds to the form of systemic mastocytosis with bone marrow and visceral involvement associated with skin disease and displays clinically aggressive behaviour. The histopathological, histochemical and ultrastructural features are described.
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PMID:Systemic mast cell disease in the Mongolian gerbil, Meriones unguiculatus: case report. 935 Jul 9

Skin biopsies from 13 Shar Peis showing signs of cutaneous mucinosis and 13 control dogs of different breeds with no clinical or histological evidence of skin disease were examined. One section of each tissue sample was stained with haematoxylin and eosin, and another with toluidine blue to demonstrate the sulphated acid glycosaminoglycans in mast cell (MC) granules. To investigate the MC subtypes involved, the tryptase and chymase content of mast cells was evaluated by a double enzyme-immunohistochemical staining technique. Regardless of the staining technique, a significantly lower mast cell density in the skin of Shar Peis was demonstrated. In the dermis of control dogs, we detected a median mast cell density of 31.2 MC/mm2 using the toluidine blue staining method and 27.5 MC/mm2 using the double labelling technique. In Shar Peis only 9.1 MC/mm2 were found by toluidine blue staining (P = 0.001) and 14.8 MC/mm2 by the double labelling method (P = 0.0387). The percentile distribution of mast cell subtypes was also significantly different in Shar Peis as compared to control dogs. Whereas in the dermis of control dogs the predominant mast cell subtype was the tryptase and chymase containing MC (TC-MC) (60.4%), in Shar Pei skin the only chymase containing MC (C-MC) predominated (62.2%) and the percentage of TC-MC was significantly lower (32.9%; P = 0.0016). The percentage of only tryptase containing MC (T-MC) (4.7%) was higher in Shar Peis compared to control dogs (1.9% P = 0.0178). The data obtained indicate a possible involvement of mast cell subtypes in the pathogenesis of cutaneous mucinosis. Further investigations on the pathophysiological role of mast cell subtypes may foster understanding of the pathogenesis of cutaneous mucinosis.
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PMID:Mast cell density and subtypes in the skin of Shar Pei dogs with cutaneous mucinosis. 1044 5

The possible involvement of mast cell tryptase and chymase in subepidermal bullous diseases was studied enzyme-histochemically in specimens from erythematous and vesicular skin and from non-involved skin of patients with dermatitis herpetiformis, bullous pemphigoid, erythema multiforme, infective bullous eruption and linear IgA dermatosis. Patients with pemphigus were biopsied for comparison. The immunoreactivity of chymase inhibitors, alpha1-proteinase inhibitor (alpha1-PI) and alpha1-antichymotrypsin (alpha1-AC), in mast cells was demonstrated using the sequential double staining method. Tryptase-positive mast cells were unchanged or only slightly increased in number in erythematous lesions and slightly decreased in blistering skin compared with healthy-looking skin. Only occasionally were mast cells seen in apparent contact with the basement membrane zone. Chymase-positive mast cells and the chymase/tryptase ratio steadily decreased during the development of the lesions in each subepidermal bullous disease. The percentage of alpha1-PI+ and/or alpha1-AC+ mast cells increased simultaneously, which could explain the disappearance of chymase activity. Similar results were obtained regardless of the bullous disease. The results were also similar in pemphigus, which is an intraepidermal bullous disease. In conclusion, these results show significant alterations in mast cell chymase and protease inhibitors in a range of different bullous diseases, suggesting mast cell involvement. The apparent inactivation of chymase could be due to the action of chymase inhibitors detected in numerous mast cells. However, these alterations probably reflect general inflammation rather than a specific reaction in a certain bullous disease.
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PMID:Mast cells in developing subepidermal bullous diseases: emphasis on tryptase, chymase and protease inhibitors. 1049 9

Varieties of the clinical features of mastocytoses, also called mastocytosis syndrome, are presented. The disease is characterized by excessive accumulation of mast cells, their proliferation and action in the skin and other organs, even in the central nervous system. The mastocytosis syndrome was known as early as the second half of the 19th century under the term urticaria pigmentosa, and was histologically confirmed by the presence in the dermis of metachromatic cells, i.e. Ehrlich mast cells with red-purple cytoplasmic granules visible with Giemsa or toluidine blue stains. The mastocytosis syndrome was then supposed to be a benign chronic dermatosis of childhood with spontaneous regression by adolescence. The clinically pathognomonic symptoms of Darier's sign (urtication of primary skin lesion upon rubbing) and flushing help in the diagnosis of mastocytosis syndrome. In the 1950s, there was a progression in the diagnosis of systemic mastocytosis achieved by scientists and clinicians of various specialties. Upon the discovery of many mast cell released mediators (heparin, histamine, leukotrienes, prostaglandins, proteases, cytokines), receptor functions, relationship to IgE, anaphylatoxin, etc., they were recognized as triggers of various clinical features of the mastocytosis syndrome. In this paper, different forms of cutaneous and systemic mastocytosis are described, with special reference to 'mastocytosis mucocutanea haemorrhagica' observed by one of the authors in a female infant and followed from 6 months till 2.5 years of age. The patient showed practically all the diverse forms of cutaneous mastocytosis: urticaria pigmentosa, papular, nodular, tumorous-like melanoma, vesiculobullous, erythrodermic, telangiectasia eruptiva maculosa perstans. She also suffered from nasal and rectal hemorrhage, conjunctival suggillations, plaque-like infiltrations of the glossal, oropharyngeal and laryngotracheal mucosa, episodes of flushing, and transitory apnea. It is emphasized that the diagnosis of mastocytosis syndrome may be difficult for its mimicking various other diseases. The occurence of mastocytosis syndrome from the neonatal period through adult and old age, and possibilities of symptomatic treatment and prevention of sudden death or fatalities are discussed. Familial occurrence of mastocytosis syndrome and new genetic studies that may prove highly useful for understanding the etiopathogenesis of mastocytosis syndrome are described.
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PMID:Clinical varieties of mastocytoses. 1150 29

Atopic dermatitis, a common, chronic, inflammatory skin disease that occurs with increasing prevalence, is characterized by hyperactivated cytokines of helper T cell subset 2 and is frequently associated with staphylococcal infection. An experimental animal model of atopic dermatitis induced by transgenically introduced cytokine is not available. We generated a transgenic mouse line expressing epidermal interleukin-4, a critical cytokine of helper T cell subset 2. Here we show that transgenic mice spontaneously developed a pruritic inflammatory skin disease reproducing all key features of human atopic dermatitis, including xerosis, conjunctivitis, inflammatory skin lesions, Staphylococcus aureus infection, histopathology of chronic dermatitis with T cell, mast cell, macrophage-like mononuclear cell, and eosinophil infiltration, and elevation of total serum IgE and IgG1. The onset and early progression of skin disease coincided with increased total serum IgE and IgG1. The mouse disease occurred at a 43% annual incidence rate and primarily affected the poorly haired skin: ear (100%), neck (65%), eye (53%), face (29%), tail (12%), leg (12%), and torso (6%). As a group the affected transgenic mice manifested with a skin disorder that fulfilled the clinical diagnostic criteria established for atopic dermatitis in human patients. Pending further characterization to authenticate it as a model of atopic dermatitis, this experimental animal model of pruritic inflammatory skin disease may facilitate investigations for the roles of interleukin-4 in cutaneous inflammation and skin infection in human patients.
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PMID:Expression of interleukin-4 in the epidermis of transgenic mice results in a pruritic inflammatory skin disease: an experimental animal model to study atopic dermatitis. 1167 41

Follicular dendritic cell tumor (FDCT) is a rare tumor mainly located in laterocervical lymph nodes. We report one case of mediastinal FDCT associated with a history of bullous skin disease and clinically obvious immunosuppression. This tumor was characterized by heavy mast cell infiltration. Mast cells were in close relationship with tumor cells as demonstrated by ultrastructural examination and their presence are probably related with the strong expression of mast cell chemoattractants as fraktalkine and stromal cell-derived factor-1alpha by tumor cells. The long follow-up period of more than 17 years allowed to us assess the relatively indolent evolution of this tumor characterized by three slowly growing local recurrences without metastasis.
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PMID:Follicular dendritic cell tumor of the mediastinum: expression of fractalkine and SDF-1alpha as mast cell chemoattractants. 1640 20


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