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

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 combination of cyclophosphamide treatment and Toxocara canis infection is known as an effective way of causing a high level of eosinophilia in mice. When this treatment was applied to congenitally anemic, mast cell-deficient W/WV mice, eosinophil response was far less than that of their normal littermate +/+ mice. The degree of the defective eosinophil response in the peripheral blood of W/WV mice was severer than that in the bone marrow. The defective eosinophil response of W/WV mice was completely restored by bone marrow grafting 8 weeks prior to cyclophosphamide treatment and T. canis infection. The kinetics of the recovery of eosinophil response in the bone marrow of W/WV mice after bone marrow grafting was faster than that in the peripheral blood. Chemotactic reactivity of eosinophils obtained from bone marrow or peritoneal cavity of W/WV mice was essentially comparable to that of +/+ mice. These results suggest that, in addition to the production of eosinophils in the bone marrow, mast cell-derived factors play an important role in the mediation of peripheral blood eosinophilia.
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PMID:Eosinophil response in mast cell-deficient W/WV mice. 355 34

Adverse reactions to the tricyclic antidepressant drugs imipramine and desipramine have been described and include eosinophilia, pulmonary infiltrates with eosinophilia, and elevated total serum IgE levels. The immunologic mechanism accounting for these adverse reactions has not been elucidated. This article describes a patient manifesting bronchospasm, profound eosinophilia, and elevated serum IgE levels after therapy with desipramine that resolved rapidly after withdrawal of the drug. Immunologic investigations failed to demonstrate specific IgE directed against a protein conjugate of desipramine but demonstrated the ability of desipramine to induce mast cell degranulation with direct intradermal skin challenges.
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PMID:Hypersensitivity reaction to desipramine. 359 27

Skin biopsies were taken from 63 patients with end-stage renal failure (ESRF) and 5 normal volunteers, 53 of whom were on maintenance hemodialysis (HD) and the other 10 without HD. They were examined with light and electron microscopy and subepidermal capillaries were subjected to image analysis. Thickening of the basement membrane (BM) with multilamination of the basal lamina, endothelial activation and chronic inflammatory cell infiltration with participation of mast cells were evident. The extent of these BM changes was correlated with the duration of HD, but not significantly correlated with the clinical findings indicative of arteriosclerosis. There was significant correlation between the duration of HD and mast cell proliferation or eosinophilia. We suspect that the subepidermal capillary changes represent an inflammatory reaction provoked by uremic toxins or by the repeated use of an artificial organ.
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PMID:Microangiopathic changes of subepidermal capillaries in end-stage renal failure. 360 Sep 23

The distinct features of the eosinophil include their content of large crystalloid granules which contain a number of unique basic proteins, and their capacity to selectively generate the SRS-A, sulphidopeptide leukotrienes. Eosinophil-derived products probably play an important role in the destruction of helminthic larvae but in some situations, for instance, chronic bronchial asthma and the hypereosinophilic syndrome, the cell might be responsible for considerable tissue damage. Eosinophils can be activated, in vitro, by a variety of agents which include factors associated with eosinophil maturation, mast cell products and other substances released during allergic tissue reactions and other inflammatory processes. At the present time there is growing interest in the fact that in many conditions associated with eosinophilia there is a population of light density "activated" cells which, in a variety of biological systems, respond more vigorously than normal ("normodense") eosinophils. Knowledge of eosinophils and eosinophil-associated events is growing rapidly and there is a need to modify continuously our views on the precise role(s) of the eosinophil in the light of these new findings.
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PMID:Eosinophils: role in asthma, allergy and parasite immunity. 387 May 2

A patient with mast cell disease of the small bowel is described in whom clinical, histological, and ultrastructural studies served to delineate the characteristic features of the disease. Urticaria pigmentosa, steatorrhea, eosinophilia, absence of antireticulin antibodies, and submucosal nodularity seen on radiographic study of the duodenum were the clinical characteristics. The endoscopic appearance was that of severe exudative duodenitis. The histology of the small intestinal mucosa showed crypt cell destruction and villous atrophy. Marked infiltration of the lamina propria with mast cells, eosinophils, and neutrophils was also distinctive. The enterocytes retained their columnar epithelium, confirmed on electron microscopy. The fine structural abnormalities of the mast cells are demonstrated for the first time. Degranulated mast cells predominated within the lamina propria and none was seen among the epithelial layers. The mast cell nuclei were irregular, often binuclear, and showed loss of their normal heterochromatin pattern. In their cytoplasm only few granulated bodies were seen and even more rarely inclusions with whorls and scrolls. We conclude that the clinical, histopathological, and ultrastructural appearances in mast cell disease of the small bowel are distinctive and should be used as criteria for diagnosis. Care should be taken in the evaluation of the number of mast cells since the demonstration of these cells may be affected by various fixing and staining techniques.
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PMID:Clinical, histological, and electron microscopic study of mast cell disease of the small bowel. 396 51

A single intraperitoneal injection of Ascaris cuticle caused a local eosinophilia with peak levels at 2 wk after injection. Mast cells reduced in number and size at 1 wk were found in increased numbers at 3 wk. Injection of a collagen-poor fraction of cuticle known as "cuticlin" resulted in a diminished eosinophil and mast cell response compared with injection of whole cuticle. Precipitating antibodies to soluble Ascaris cuticle collagen were detected in the serum and peritoneal fluid from day 5 onward. It is proposed that the eosinophilia and mast cell hyperplasia are the result of immunization of the animal to an antigen present in Ascaris collagen and rendered soluble by the action of mononuclear phagocytes. The eosinophil and mast cell response to Ascaris cuticle mimicked the response in connective tissue to living nematode parasites. It is concluded that the cuticle of nematode parasites may be responsible for eosinophilia and mast cell hyperplasia in the host.
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PMID:Eosinophilia, mast cell hyperplasia and antibody production in rats following an intraperitoneal injection of Ascaris cuticle including in-vitro studies of immune eosinophil granule lysis. 400 Jul 8

The role of mast cells in induction of uterine eosinophilia was investigated by using genetically mast cell-deficient (WB X C57BL/6)F1-W/Wv (hereafter called WBB6F1-W/Wv) mice. The injection of estradiol-17 beta (0.16 micrograms/g body weight) increased the peroxidase activity and eosinophil number in the uteri of castrated WBB6F1-W/Wv and WBB6F1-+/+ mice. Since no significant differences were detectable between these two type of mice, mast cells did not seem to be essential for the estrogen-induced uterine eosinophilia, at least in mice.
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PMID:Estrogen-induced increase in eosinophil number and peroxidase activity in uterus of genetically mast cell-deficient W/Wv mice. 408 34

The effects of peripheral eosinophilia on the intensity, kinetics and cellular characteristics of rat cutaneous late-phase reactions (LPR) have been investigated. Two distinct methods of inducing peripheral eosinophilia did not alter either the intensity or the kinetics of LPR produced by the intradermal injection of anti-IgE, Compound 48/80, or isolated mast cell granules. Hypereosinophilic animals exhibited increased numbers of tissue eosinophils in LPR tissue sites which correlated with the elevations in their respective peripheral eosinophil counts; however, the absolute number of eosinophils present, although significant, was not impressive (less than 10% of total). Our data suggest that, although rat LPR can be modulated to involve increased tissue eosinophils by increasing the numbers of peripheral blood eosinophils, no effects of these procedures on altering either the intensity or the kinetics of these reactions can be appreciated.
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PMID:The experimental production of increased eosinophils in rat late-phase reactions. 617 27

This study examined the elevation of blood eosinophil counts in athymic and thymus-intact mice after repeated injections of polymyxin B with and without infection by Schistosoma mansoni. In athymic mice, a modest, comparable eosinophilia occurred after polymyxin B injection or parasite infection alone, or after a combination of both. In thymus-intact mice, polymyxin B injection caused a similar low grade eosinophilia, and schistosome infection produced a much higher level of eosinophilia. The combination resulted in the highest levels during the early weeks after infection; this hyperresponsive phenomenon was most apparent following 5 to 7 weekly polymyxin B injections, and the total eosinophil count approximated that derived by adding the eosinophil counts induced by polymyxin B injections or schistosome infection alone. In spite of the changes in blood eosinophil counts, tissue eosinophilia in the liver revealed no apparent differences. Furthermore, in schistosome-infected and polymyxin B-injected thymus-intact mice, hepatic granulomas reached a maximal size earlier than in mice that were only infected, and there was an over-all reduction in mast cell counts. The findings indicate that a T cell-independent eosinophilia occurs under a variety of circumstances. In athymic mice, it accounts for all peripheral eosinophilia, whereas in thymus-intact mice, it operates independently from the well known T cell-dependent eosinophilia of parasite infections.
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PMID:Induction of T cell-independent eosinophilia in mice with polymyxin B and schistosome infection. 625 55


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