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)

Platelet factor 4 (PF4) has previously been linked to precipitation of cold urticaria (CU). The aim of the study was to assess the liberation of PF4, eosinophil cationic protein (ECP) and histamine after cold challenge in patients with CU. Ten controls and 8 patients with CU verified by clinical data and cold challenge test were investigated. Assessment of histamine, ECP and PF4 were done using radioimmunoassays. In patients histamine increased after 10 min on the challenged arm (NS), PF4 increase was statistically significant (p less than 0.05) both in patients and controls. ECP release showed no significant changes. Treatment with doxepin results in clinical improvement, but no changes in mediator release were seen. Thus, in contrast to previous reports an increase of PF4 was seen both in controls as well as in patients. An involvement of ECP was not ascertained. Our data suggest that neither basophils, nor eosinophils or platelets are directly involved in cold urticaria and that mast cell-dependent mediators may be of greater relevance.
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PMID:Cold urticaria as a model of mediator release: platelet factor 4, eosinophil cationic protein and histamine. 128 Sep 16

We studied the role of atopy, as defined by positive skin tests to common inhalant allergens, in allergic bronchial inflammation. Endobronchial biopsies were taken via the fibreoptic bronchoscope in 13 symptomatic atopic asthmatics, 10 atopic nonasthmatics, and 7 normals. The numbers of mast cells, identified in the submucosa by immunohistochemistry using the AA1 monoclonal antibody against tryptase, were no different between the three groups, but electron microscopy showed that mast cell degranulation, although less marked in atopic nonasthmatics, was a feature of atopy in general. The numbers of eosinophils, identified by immunohistochemical staining using the monoclonal anti-eosinophil cationic protein antibody, EG2, were greatest in the asthmatics, low or absent in the normals and intermediate in the atopic nonasthmatics. In both atopic groups eosinophils showed ultrastructural features of degranulation. Measurements of subepithelial basement membrane thickness on electron micrographs showed that the collagen layer was thickest in the asthmatics, intermediate in the atopic nonasthmatics and thinnest in the normals. The results suggest that airways eosinophilia and degranulation of eosinophils and mast cells, as well as increased subepithelial collagen deposition, are a feature of atopy in general and suggest that the degree of change may determine the clinical expression of this immune disorder.
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PMID:Bronchial mucosal manifestations of atopy: a comparison of markers of inflammation between atopic asthmatics, atopic nonasthmatics and healthy controls. 161 55

The knowledge about the differentiation of basophilic leukocytes is fragmentary. This report discusses a detailed phenotypic characterization of molecular markers for hematopoietic differentiation in a basophilic leukemia cell line, KU812. The expression of markers for lymphoid, erythroid, neutrophil, eosinophil, monocytic, megakaryocytic, mast cell and basophil differentiation was analyzed at the mRNA level by Northern blots in the KU812 cells, and for reference, in a panel of human cell lines representative of the different hematopoietic differentiation lineages. KU812 was found to express a number of mast cell and basophil-related proteins, i.e. mast cell tryptase, mast cell carboxypeptidase A, high-affinity immunoglobulin (IgE) receptor alpha and gamma chains and the core protein for heparin and chondroitin sulphate synthesis. We found no expression of a number of monocyte/-macrophage or neutrophil leukocyte markers except for lysozyme. From earlier studies, it has been shown that lysozyme is not expressed in murine mucosal mast cell lines. This finding, together with the expression of the mast cell carboxypeptidase in KU812 might distinguish the phenotype of this cell line from that typical of mucosal mast cell lines in rodents. We found a low level of expression of the eosinophil and basophil marker, major basic protein, which might indicate a relationship between basophils and eosinophils. No expression is, however, detected with the eosinophil-specific markers eosinophil cationic protein, eosinophil-derived neurotoxin or eosinophil peroxidase. We also report an extensive screening for inducers of basophilic differentiation of the KU812 cells. The most efficient protocol of induction included serum starvation which led to a dramatic increase in a number of markers specific for mast cells and basophils such as tryptase, carboxypeptidase A and the heparin core protein. Finally, diisopropylfluorophosphate analysis of total protein extracts from KU812 show four labeled protein bands with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, indicating that this cell line expresses at least three previously undescribed serine proteases of which one or more could be a potential basophil-specific marker(s).
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PMID:Phenotypic characterization of KU812, a cell line identified as an immature human basophilic leukocyte. 163 3

Eosinophil cationic protein (ECP) is a protein specific to the granules of human eosinophil granulocytes, ECP is highly cationic and may damage tissue if not inactivated. Heparin is a highly anionic substance present in mast cells and basophil granulocytes. The present in vitro study shows that ECP can inactivate the anticoagulant activity of heparin probably by the formation of a complex between the two molecules. This function may be of importance for the microenvironment of allergic diseases where secretion of heparin may promote penetration of mast cell products through tissues. Also this may constitute one mechanism whereby the cytotoxic action of ECP is neutralized.
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PMID:In vitro studies of the interaction between heparin and eosinophil cationic protein. 201 6

We have used fiberoptic bronchoscopy to obtain endobronchial biopsies in which mast cells and eosinophils were enumerated using monoclonal antibodies directed against mast cell tryptase (AA1) and the eosinophil cationic protein (EG2). Eleven symptomatic atopic asthmatics treated with beta 2-agonists alone and six normal subjects were studied. Over a period of 2 wk prior to bronchoscopy, patients recorded asthma symptom scores, bronchodilator usage, and twice-daily peak expiratory flow. Five days before bronchoscopy, methacholine responsiveness was assessed. Two biopsies were taken from the subcarinae, one of which was processed into araldite for immunostaining by the streptavidin biotin immunoperoxidase method and the other into Spurr resin for electron microscopy. The number of AA1 staining mast cells present in the bronchial mucosa was not significantly different in the epithelium or submucosa between the asthmatic and the normal subjects. However, in the biopsies from asthmatics, there were significantly greater numbers of EG2-staining eosinophils in the epithelium (median, 1.2/mm versus zero; p less than 0.005) and in the submucosa (median, 50/mm2 versus 1/mm2; p less than 0.001). Electron microscopy showed morphologic features of mast cell and eosinophil degranulation in the asthmatics. No correlation could be established between mast cell or eosinophil numbers and indices of disease activity of PC20 methacholine, which points to the complexity of mechanisms responsible for the symptoms and the airway hyperresponsiveness of asthma.
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PMID:Quantitation of mast cells and eosinophils in the bronchial mucosa of symptomatic atopic asthmatics and healthy control subjects using immunohistochemistry. 202 38

Painful bladder disease is an ill-defined disease presenting with chronic cystitis symptoms, despite sterile urine. This report includes only patients with painful bladder diseases of unknown etiology and pathogenesis. We have chosen to classify these patients pathoanatomically as follows: interstitial cystitis, detrusor myopathy, chronic unspecific cystitis and eosinophilic cystitis. The pathoanatomical appearance of the four groups of patients are described in details and certain clinical differences appear between the groups. The etiology and pathogenesis to the inflammatory reactions and muscle changes found in the detrusor biopsies are unknown, but many theories exist. It is suggested that something in the urine gains access to the bladder wall and initiates the pathoanatomical changes through a defective urothelium and glycosaminoglycans layer. In the interstitial cystitis patients, the inflammatory process and mast cell degranulation might be monitored by the urinary excretion of 1,4-methyl-imidazole-acetic acid and eosinophil cationic protein. It is concluded that no specific therapy for the disease exists, since etiology and pathogenesis are still unknown and therefore future research in this field is very important.
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PMID:Pathology and pathophysiology of painful bladder diseases. 262 83

A diagrammatic representation of the interactions between mediators of hypersensitivity and leucocytes in early-, late-phase, and ongoing asthma is shown in Fig. 1. Early-phase or immediate reactions are largely the result of bronchoconstriction consequent to the release of mediators such as histamine, PGD2, LTC4/D4 and PAF. The principal mediator cell (MC) is the mast cell (although other IgE receptor-bearing cells such as the macrophage, eosinophil and platelet might also be involved in this immediate response). The stimulus for mediator cell activation may be either immunologic (IgE-dependent) or non-immunologic (i.e. changes in osmolarity as a result of the respiratory water loss associated with exercise-induced asthma). Late-phase reactions appear to be a consequence of infiltration with neutrophils (N), eosinophils (E) and macrophages (MO). These cells are recruited and activated either by mast cell-associated chemotactic factors [such as LTB4, PAF, the eosinophil chemotactic factor of anaphylaxis (ECF-A) or high molecular weight neutrophil chemotactic activity (NCA (HMW]] and/or "lymphokines" derived from T helper cells (TH) which have been stimulated by antigen processed by the antigen processing cells (APC). These mononuclear cell interactions are under the control of regulatory T cells [T suppressor (TS) cells] and it is speculated that the availability of these subsets may determine the magnitude of the late-phase response. Lymphokines and monokines which selectively activate neutrophils, eosinophils and monocytes include LIF, EAF and INF-gamma respectively. Macrophage-derived tumour necrosis factor (TNF) also amplifies the inflammatory response by its capacity to enhance eosinophil cytotoxicity. Eosinophil-derived agents such as PAF, LTC4, MBP and ECP might be responsible for submucosal oedema and non-specific bronchial hyperreactivity which are characteristic features of late-phase reactions. T cell-derived lymphokines such as EDF (IL-5), together with GM-CSF, might lead to eosinophilopoiesis and account for the prolonged eosinophilia of ongoing chronic asthma. The T cell is prominent in the pathology of chronic asthma and is possibly "chronically activated". Thus lymphocytes, driven by as yet undetermined "antigens" (possibly viral), may perpetuate the inflammatory response in and around the bronchi. IL-5-like products from these putative activated lymphocytes might perpetuate (a) eosinophil production by the bone marrow, (b) its release into the circulation, (c) its migration into bronchial tissue and (d) activation to release PAF, LTC4, MBP, etc.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Leucocytes in asthma. 306 26

The role of the eosinophilic granulocyte in immediate hypersensitivity reactions is generally believed to be a beneficial one since this cell may phagocytose mast cell granules and inactivate certain mast cell mediators. However it has become clear that the eosinophilic granulocyte also has potent secretory capacities, and by this property may contribute in a detrimental way to the allergic process. In studying the late phase allergen induced bronchoconstriction by means of bronchoalveolar lavage (BAL) an evident infiltration of eosinophilic granulocytes in the bronchioli in the beginning of the late phase asthmatic reaction was noticed. Since also eosinophil cationic protein (ECP) has been reported to be elevated in the lavage fluid an active secretory role of the eosinophil in the late phase asthmatic reaction seemed likely. Although the release of ECP and other granular proteins may contribute to epithelial damage and inflammation and thereby to an increase in bronchial hyperreactivity they do not explain the late phase bronchoconstrictive reaction. Since leukotrienes were thought possible candidates to cause this reaction it was decided to isolate eosinophils from human peripheral blood and to study their leukotriene synthesis pattern. To our surprise purified human eosinophils almost exclusively synthesize the strongly bronchoconstrictive leukotriene LTC4 in considerable quantities upon in vitro stimulation with either the calcium-ionophore A23187 or opsonized zymosan. These findings suggest that the eosinophil may play an active role in causing the late phase asthmatic reaction.
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PMID:The eosinophilic granulocyte an active participant in the late phase asthmatic reaction? 308 93

Immuno-histopathological studies of conjunctival tissue biopsied from patients with non-sight-threatening allergic conjunctivitis or with sight-threatening allergic keratoconjunctivitis should lead to more effective management of these eye conditions, based on the specific cellular involvement. The major difference between these two categories of eye disease was the occurrence of T-lymphocytes, which were absent in the former but prominent in the sight-threatening disorders. Seasonal and perennial allergic conjunctivitis both showed a heavy mast cell increase, due to infiltration of mucosal type mast cells, and allergen challenge studies linked mast cell histamine release to the early phase reaction occurring within 20 minutes. A second histamine peak at six hours after challenge might implicate basophils (or refractory mast cells) and was accompanied by a rise in eosinophil cationic protein. In sight-threatening, chronic allergic keratoconjunctivitis the responses were clearly directed by T-cells, themselves the primary effector cell in atopic keratoconjunctivitis, whereas vernal keratoconjunctivitis displayed a T-cell driven eosinophilia, with increased expression of the adhesion molecules involved in tissue invasion by these cells. Appropriate therapies for each different category of conjunctivitis should be based on the specific immunopathology, and directed at the activated cell types that are primarily responsible for the disease process.
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PMID:Therapeutic considerations: symptoms, cells and mediators. 754 Mar 64

In both seasonal and perennial rhinitis there is epithelial mast cell accumulation and tissue infiltration by eosinophils. Activation of these cells can be observed by electron microscopy and by elevated levels of tryptase and eosinophil cationic protein in nasal lavage fluid. Furthermore, seasonal increases in the antigen presenting cell (Langerhans' cell) are also evident. Investigations into the mechanisms involved in cell accumulation and activation reveals upregulation of leucocyte endothelial adhesion molecules and an increase in interleukin-4 (IL-4) in naturally occurring rhinitis, while mRNA for IL-4, IL-5 and granulocyte macrophage colony stimulating factor activity and lavage tumour necrosis factor-alpha (TNF alpha) levels are increased following local allergen challenge. These cytokines may be derived from a variety of sources, including mast cells, eosinophils and T-lymphocytes, and contribute to the underlying inflammatory process in rhinitis.
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PMID:The cellular basis for allergic rhinitis. 760 53


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