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)

A group of male Wistar rats (strain AF/HAN) received carrageenin in a tragacanth suspension and saline solution by subplantar injection into the right and left hind paws, respectively. Another group was treated similarly with Mycobacterium butyricum in Freund's adjuvant given in the right hind paw while the left paw served as control. The experiments ran for 20 days. The paw volume was measured plethysmometrically and general histological examination was carried out on samples of the dorsal paw epidermis and dermis. The mast cell count and thickness of epidermis were also determined. Epidermal and dermal changes developed in distinct stages following carrageenin or adjuvant treatment. During the acute phase (from 0 to 12 h post-treatment) the paw volume as well as the thickness of the epidermis increased while the dermal mast cell count decreased. Furthermore, hyperemia, edema and leukocytic infiltration of the connective tissue was observed. Eosinophilia and focal necrosis appeared only in the adjuvant treated animals. In the subacute phase (from 1 to 3 days post-treatment) paw swelling and epidermal hyperplasia recessed slightly in the carrageenin treated group. On the other hand, paw volume of the adjuvant treated animals continued to rise. These changes were accompanied by proliferative and degenerative processes of the connective tissue (fibroplasia, histiolymphocytic infiltration, focal necrosis). A chronic phase of inflammation (from 4 to 20 days post-treatment) developed only in the adjuvant treated group. Epidermal hyperplasia reappeared and the paw volume increased significantly (secondary reaction). Also granulomatous chronic inflammation and foreign-body giant cells proliferated in the connective tissue.
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PMID:[Histometrical studies on induced paw inflammation by carrageenan and Freund's complete adjuvant in rats]. 76 65

Sixteen bone marrow aspirates and 15 trephine core biopsies from 17 children with cutaneous mastocytosis, of which 15 exhibited urticaria pigmentosa and 2 exhibited diffuse cutaneous mastocytosis, were evaluated for the presence of bone marrow-associated pathologic conditions. Eight bone marrow aspirates from 8 children and 23 trephine core bone marrow biopsies from 16 children who had had evaluation for hematologic abnormalities not associated with cutaneous mastocytosis served as a control population. Eosinophilia was a prominent finding in bone marrows of 9 of 17 patients who had cutaneous mastocytosis. Increased mast cell numbers in bone marrow aspirates were observed in 5 children with cutaneous mastocytosis (5 of 16) and in 2 of the control children (2 of 8). Examination of the trephine core bone marrow biopsies obtained from patients with cutaneous mastocytosis demonstrated focal perivascular and paratrabecular aggregates consisting of mast cells, eosinophils, and early myeloid cells in 10 of 15 individuals. Similar lesions were observed in trephine core bone marrow biopsies of 3 of 16 control patients. The focal mast cell lesions characteristic of adult systemic mastocytosis were not observed. The authors conclude that cutaneous mastocytosis in the pediatric age group is rarely associated with definitive bone marrow findings suggestive of systemic mast cell disease and that this observation is consistent with previous reports that cutaneous mastocytosis in the majority of pediatric cases resolves by adulthood.
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PMID:Hematopathology of the bone marrow in pediatric cutaneous mastocytosis. A study of 17 patients. 247 Feb 48

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

Abomasal mucosal mast cell and eosinophil accumulation was morphometrically evaluated in 26 Holstein steers after natural or experimental infection with Ostertagia ostertagi. Results showed that following infection, accumulation of mast cells and eosinophils in abomasal tissue was dependent on infection pattern. Eosinophilia was greater in steers with type 1 ostertagiosis, while mastocytes was more pronounced in steers with type 2 ostertagiosis.
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PMID:Cellular and chemical mediators of type 1 hypersensitivity in calves infected with Ostertagia ostertagi: mast cells and eosinophils. 835 82

Studies of the pathology of rhinitis and asthma have identified similarities and differences between these two clinical conditions. With regard to symptoms, both the nose and the lower airways respond to neural stimulation by irritant substances, but a major difference is that engorgement of the capacitance vessels is the main cause of nasal obstruction in rhinitis, while muscle constriction is the major determinant of lower airway narrowing. There are also similarities and differences with respect to the role of inflammatory cells. In both conditions there is evidence of allergen-induced mast cell activation, with production of an array of mediators (some mast cell-derived and others originating from a variety of other cell types). Eosinophilia is also characteristic of both diseases--it is prominent even in mild forms of asthma, but is low in pollen-sensitive rhinitics outside of the season. T-cell activation and production of cytokines plays an important role in the development and maintenance of allergic disease, but the level of T-cell activation may differ between asthma and rhinitis. Further research into differences in cellular activity and response to treatment between these two diseases may help define factors which will determine whether atopic disease is expressed in the upper, lower, or both parts of the respiratory tract.
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PMID:Pathology of rhinitis and bronchial asthma. 873 59

Eosinophilia is a feature of airway inflammation associated with asthma. Leukotriene antagonists provide therapeutic benefit in asthma, but their potential antiinflammatory actions have not been fully explored. We have examined the role of eosinophil-derived cysteinyl leukotrienes in the maintenance of eosinophil survival, and the involvement of leukotrienes in the paracrine stimulation of eosinophil survival by mast cells and lymphocytes. We obtained eosinophils and autologous lymphocytes from peripheral blood of asthmatic subjects. Leukotriene (LT)-B(4), LTC(4) and LTD(4), granulocyte-macrophage colony-stimulating factor (GM-CSF), and fibronectin promoted eosinophil survival. LTD(4) (10(-)(6) M) was as effective as GM-CSF (5 ng/ml) and fibronectin (400 ng/ml) in promoting survival. Lymphocytes and conditioned medium from a human mast cell line (HMC-1) induced eosinophil survival. Blockade of cysteinyl leukotriene receptors with SKF 104353 (pobilukast, 3 nM), and inhibition of 5-lipoxygenase (5-LO) with BW A4C (1 microM) and of 5-LO activating protein with MK 886 (1 microM), all increased basal rates of eosinophil apoptosis and reversed GM-CSF-induced eosinophil survival. Fifty percent reversal of GM-CSF- induced survival was achieved with SKF 104353 at 0.3 nM. The potency of SKF 104353 was two orders of magnitude greater than that of the LTB(4) receptor antagonist SB 201146. Mast cell- and lymphocyte-induced eosinophil survival were completely reversed by SB 201146, SKF 104353, BW A4C, and MK 886. These findings provide evidence for the involvement of an autocrine cysteinyl leukotriene pathway that supports eosinophil survival in response to a range of survival stimuli. They also suggest that LTB(4) could act as a paracrine stimulus of eosinophil survival.
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PMID:Leukotriene receptor antagonists and synthesis inhibitors reverse survival in eosinophils of asthmatic individuals. 1085 61

Disodium cromoglycate is an anti-asthmatic drug that has mast cell-stabilizing effects and other anti-inflammatory effects. However, the mechanisms of its anti-inflammatory effects are unclear. In this study, we evaluated effects of disodium cromoglycate on eosinophilia, early and late asthmatic responses, and production of arachidonic acid metabolites in guinea pig lungs. Guinea pigs were alternately sensitized and challenged by exposure to mists of ovalbumin+Al(OH)(3) and ovalbumin, respectively. Disodium cromoglycate (0.5-2 mg/0.1 ml/animal) administered intratracheally before the fifth challenge dose-dependently inhibited asthmatic response, but early asthmatic response was not affected. Disodium cromoglycate at 2 mg/animal potently suppressed increases in cysteinyl leukotrienes (CysLTs) and thromboxane A(2) in the lung during late asthmatic response. Eosinophilia was slightly reduced by disodium cromoglycate. The inhibitory effect of disodium cromoglycate on late asthmatic response is apparently due to inhibition of the release of arachidonic acid metabolites, some of which may be derived from eosinophils that infiltrate the lung.
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PMID:Intratracheal dosing with disodium cromoglycate inhibits late asthmatic response by attenuating eicosanoid production in guinea pigs. 1532 40

A 12-year-old Arab stallion was presented with a chronically swollen right carpus resulting in profound lameness of the same leg. An incisional biopsy of subcutaneous tissue from the right carpus submitted for cytology and histopathology revealed large numbers of eosinophils interspersed by substantial numbers of variably sized and granulated mast cells. Fungal culture of a subcutaneous tissue sample taken from the right carpus was negative. Serial full blood counts revealed persistent mature eosinophilia, not accompanied by a mastocytaemia, neutrophilia without left shift and persistent hyperfibrinogenaemia. After humane destruction, dissection of the affected limb revealed a thick layer of connective tissue deposited around the right carpal joint. Within the connective tissue were embedded many small 0.25-1 cm diameter yellow gritty nodules, which consisted of dystrophic calcification and necrotic cell debris. The tendons enveloped by the connective tissue mass had limited function. The right axillary lymph node was moderately enlarged, yellow-brown and moist. Histopathological examination revealed a moderately well differentiated mast cell neoplasm with evidence of metastasis to the regional lymph node. In horses, malignant mast cell neoplasia is rare, while metastasis has only been reported in one other horse. Eosinophilia associated with equine mast cell neoplasia has not been reported previously but is recorded in mast cell neoplasia in the dog.
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PMID:Malignant mast cell neoplasia with local metastasis in a horse. 1603 86

Eosinophilia is a recurrent feature and diagnostic clue in several hematologic malignancies. In stem cell- and myelopoietic neoplasms, eosinophils are derived from the malignant clone, whereas in lymphoid neoplasms and reactive states, eosinophilia is usually triggered by eosinopoietic cytokines. Myeloid neoplasms typically presenting with eosinophilia include chronic myeloid leukemia, chronic eosinophilic leukemia (CEL), other myeloproliferative neoplasms, some acute leukemias, advanced mast cell disorders, and rare forms of myelodysplastic syndromes. Diagnostic evaluations in unexplained eosinophilia have to take these diagnoses into account. In such patients, a thorough hematologic work-up including bone marrow histology and immunohistochemistry, cytogenetics, molecular markers, and a complete staging of potentially affected organ systems has to be initiated. Endomyocardial fibrosis, the most dangerous cardiovascular complication of the hypereosinophilic state, is frequently detected in PDGFR-mutated neoplasms, specifically in FIP1L1/PDGFRA+ CEL, but is usually not seen in other myeloid neoplasms or reactive eosinophilia, even if eosinophilia is recorded for many years. Treatment of hypereosinophilic patients depends on the variant of disease, presence of end organ damage, molecular targets, and the overall situation in each case. In a group of patients, oncogenic tyrosine kinases (TK) such as FIP1L1/PDGFRA, can be employed as therapeutic targets by using imatinib or other TK-blocking agents.
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PMID:Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders. 1924 39

Eosinophilia in clinical practice can occur due to various pathologic processes. Causes of eosinophilia include idiopathic eosinophilia, reactive eosinophilia, idiopathic hypereosinophilic syndrome (HES), chronic eosinophilic leukemia, and other hematopoietic neoplasms (myeloid, lymphatic, or mast cell). We present a case of a 22-year-old man with HES with remarkable clinical manifestations and treatment challenges.
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PMID:Management of F/P+/- hypereosinophilic syndromes: case report and treatment review. 2072 10


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