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)

The sera of 4 patients with bullous pemphigoid, of 5 patients with drug reactions and of 13 patients with atopic eczema were examined for the occurrence of low molecular weight eosinophil chemotactic factor (ECF) by fractionation on a Sephadex G 25 column. Almost all patients had a peripheral eosinophilia, and many had raised total serum IgE levels. ECF was demonstrated in the sera of all 4 patients with bullous pemphigoid and in 4 of 5 patients with systemic drug reactions. In contrast, the sera of the 13 patients with atopic eczema did not contain any ECF activity, nor did the 13 control sera. These findings suggest that the ECF from phagocytosing polymorphonuclear leukocytes (PMN) and/or the mast cell derived ECF-A contribute to the elevated serum ECF levels in patients with bullous pemphigoid and drug reactions. A correlation between serum ECF and IgE levels and peripheral eosinophilia could not be established.
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PMID:Serum eosinophil chemotactic factor levels in patients with bullous pemphigoid, drug reactions and atopic eczema. 15 67

A West Indian man who was infected with Strongyloides stercoralis developed small intestinal obstruction. Treatment with thiabendazole did not relieve the obstruction which was found at laparotomy to be due to a poorly differentiated small intestinal lymphoma. There was no blood eosinophilia or accumulation of eosinopohils in the sites of infection. There was no reaction in the skin to delayed hypersensitivity antigens and the blood T lymphocyte count and serum C3 levels were low. From these findings and a review of the literature it was concluded that the immune response in man to Strongyloides stercoralis may depend on T lymphocyte mediated reactions including granuloma formation, and mast cell and eosinophil responses in tissues. We suggest that the association of strongyloides hyperinfection and small bowel lymphoma in this patient may not have been fortuitous. The lymphoma may have led to a reduction in cellular immunity, with the subsequent development of strongyloides hyperinfection.
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PMID:Strongyloides stercoralis infection and small intestinal lymphoma. 31 39

The gut wall is one of the conspicuous sites of eosinophil accumulation, presumably because of local chemotactic stimuli. It is reasonable to assume that one chemotactic factor is released by the mast cell, which is often found in proximity to the eosinophil. The association of eosinophils and eosinophilia with allergic disorders has long been recognized, and recent work has shown that increased eosinophil production is mediated by the lymphocyte. That process shares characteristics with other immunological actions. An increased rate of eosinophil tissue accumulation and destruction may be the factor which initiates the mechanism for increased production. None of many hypotheses about the 'function' of the eosinophil is substantiated; nevertheless it seems likely that this member of the immunological apparatus, which tends to be distributed in the front line (mucosal and cutaneous tissues), fulfils some normal protective or homeostatic function. Aside from that assumed normal function, there is growing clinical evidence that eosinophils can at times cause host injury, for example in such states as eosinophilic gastroenteritis and endomyocarditis.
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PMID:Immunology of the gut: role of the eosinophil. 34 22

A peptide of approximately 300-400 daltons exhibiting in vitro chemotactic activity for human polymorphonuclear (PMN) leukocytes, with a preference for the eosinophil series, was isolated from extracts of anaplastic lung carcinomas of the large squamous cell type obtained from three patients with marked peripheral blood hypereosinophilia and eosinophilic infiltration of the tumors and surrounding normal pulmonary tissues. This chemotactic factor was termed ECF-LSC (eosinophil chemotactic factor of lung squamous cell carcinoma). ECF-LSC appeared in the urine of two of the patients in increasing quantities late in the course of their disease and was also elaborated by long-term cultures of dispersed tumor cells from the same two patients. Three anaplastic large cell bronchogenic carcinomas which were not associated with tumor tissue or peripheral blood eosinophilia, a bronchogenic adenocarcinoma from a patient with only peripheral eosinophilia, and a renal cell carcinoma metastatic to the lungs and associated with transient pleural tissue and fluid eosinophilia were all devoid of ECF-LSC. ECF-LSC from tumor tissue extracts, urine, and tumor cell culture medium was comparable to the mast cell-associated tetrapeptides of the eosinophil chemotactic factor of anaphylaxis (ECF-A) in size, but eluted from Dowex-1 at pH 5.0-3.5 in contrast to the more acidic ECF-A tetrapeptides which eluted at pH 3.2-2.2 ECF-LSC, like the tetrapeptides of ECF-A, had a secondary chemotactic activity for neutrophil PMN leukocytes, but not mononuclear leukocytes, and deactivated both eosinophil and neutrophil PMN leukocytes so that they would not respond to a subsequent in vitro chemotactic stimulus. Eosinophils from the two patients with urinary excretion of ECF-LSC and the highest concentrations in tumor extracts were hyporesponsive in vitro to homologous and heterologous chemotactic stimuli, suggesting that ECF-LSC had deactivated the eosinophils in vivo.
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PMID:Production of a low molecular weight eosinophil polymorphonuclear leukocyte chemotactic factor by anaplastic squamous cell carcinomas of human lung. 64 Nov 54

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

Phospholipid preparations from the nematode Ascaris suum or cysts of Echinococcus granulosus (hydatid cysts) induced an eosinophilia when injected into the peritoneal cavity of rats. Peritoneal eosinophilia persisted throughout 21 days of daily injections of Ascaris lipid and was accompanied by blood eosinophilia, mast cell granule lysis and mast cell hyperplasia. The active material consisted of lecithin and lecithin plasmalogen, and in aqueous suspension had a membrane-like appearance. Electron microscopy revealed that the phospholipid was ingested by all types of cells in the peritoneal cavity, including mast cells, and was rapidly broken down by eosinophils. Phagocytosis was found to be complement dependent. The lipid combined with properdin in human serum and stimulated complement breakdown via the alternative complement pathway.
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PMID:Eosinophilia and mast cell hyperplasia induced by parasite phospholipid. 87 90

In an active cutaneous anaphylaxis induced by DNP-ascaris extract in guinea-pig, tissue eosinophilia manifested two phases; the early and mild phase became maximal in about 6 h, while the delayed and intense phase in 18-24 h. Skin extracts from the lesions exhibited chemotactic activities for eosinophils, respectively comparable to the intensity of tissue eosinophilia in each phase; and two different chemotactic factors for eosinophils of skin extracts were separated by gel filtration on Sephadex G-100. The mediation of the early phase seemed to be associated with a thermostable factor with amolefular weight of less than 1400; this factor seemed to be related to mast cell degranulation. The mediation of the delayed phase appeared to be associated with a thermolabile factor with a molecular weight of about 70,000, probably independent of mast cell degranulation; the factor was considered to be more significant than the thermostable factor, because the delayed tissue eosinophilia was more intense than the early tissue eosinophilia.
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PMID:The mediation of tissue eosinophilia in hypersensitivity reaction. I. Isolation of two different chemotactic factors from DNP-Ascaris extract-induced skin lesion in guinea-pig. 126 51

Bone marrow cell composition in male Wistar rats exposed to long-term continuous (Run 1) or interrupted (Run 2) hypo-geomagnetic field (HGMF) with an attenuation coefficient of 172.5 generating in a permalloic chamber has been studied. When comparing the rat myelograms of the two test runs, a significant increase of lymphoid cell content, less pronounced during an interrupted exposure to HGMF by 10.1 and 6.5%, respectively, was noted. Analysis of myeloid cell response indicated that on a continuous exposure to HGMF the percentage of neutrophilic promyelocytes and myelocytes is somewhat declined. The levels of mature relating to stab and nuclear-segmental neutrophils in bone marrow during both modes of HGMF exposures practically remained unchanged. A certain decrease in cell fractions of erythroblastic shoot (chiefly at the cost of polychromatophilic normocytes), to a lesser extent manifested during an interrupted exposure to HGMF (by 5.8 and 2.4%, respectively) was noted. Long-term exposure of the animals to a weak terrestrial magnetic field causes a particular eosinophilia of bone marrow due to an increased fraction of mature eosinophils approximately similar on both HGMF profiles (by 2.1 and 2.0% respectively). On an interrupted HGMF exposure there was a significant myelogram elevation of the mast cell counts by 1.4%.
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PMID:[The comparative characteristics of the bone marrow cellular composition in rats after the prolonged continuous or interrupted action of a low geomagnetic field]. 129 48

The efficacy of cetirizine in comparison with meclizine, another piperazine H1 receptor antagonist, in rat pleurisy caused by allergen or autacoid was investigated. Sensitization was achieved by subcutaneous injection of a mixture of ovalbumin and aluminium hydroxide. Fourteen days later, the animals were challenged with an intrathoracic injection of ovalbumin (12 micrograms/cavity), which caused drastic mast cell degranulation, followed by pleural oedema and leucocyte influx. Cetirizine and meclizine (2.5-30 mg/kg i.p.), 1 h before challenge, inhibited the exudatory response evoked by antigen, under conditions where neutrophil and eosinophil accumulation was affected only by the former. When administered intrathoracically 22 h after allergen, i.e. using a curative approach, cetirizine (15 micrograms/cavity) drastically reduced the pleural eosinophilia noted 24 h post-challenge, indicating that this drug can reverse an already established eosinophilia. Cetirizine (15 mg/kg i.p.) also restored, to about 39% (P < 0.001), the number of uninjured mast cells recovered from the pleural cavity following allergen stimulation. In normal rats, cetirizine (5-15 micrograms/cavity) completely inhibited the pleural exudation elicited by histamine and only partially the exudation caused by 5-hydroxytryptamine or bradykinin, but was quite inactive against platelet-activating factor. We conclude that the pleural exudation triggered by allergen, vasoactive amines or bradykinin is clearly sensitive to cetirizine. In addition, the ability of the drug to interfere with pleural neutrophil or eosinophil mobilization and mast cell degranulation seems not to be associated with its ability to block the histamine H1 receptor.
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PMID:Suppression by cetirizine of pleurisy triggered by antigen in actively sensitized rats. 136 60

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


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