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)

Neutrophil and eosinophil chemotactic activities (NCA and ECA) were measured in serum from twenty-two patients with urticaria pigmentosa or systemic mastocytosis. NCA was also measured after heating serum to 56 degrees C (heat-stable NCA). Although these factors were increased in about half of the patients there was no correlation with histamine release as estimated by the excretion of the main histamine metabolite methylimidazoleacetic acid (MelmAA) in urine. A significant increase in heat-stable NCA, however, was found in patients with pruritus and abnormal high values of MelmAA. It is concluded that only heat-stable NCA is a specific mast cell mediator, but that the heat-labile NCA and ECA are dependent on mast cells for their production by a different cell, tentatively identified as the macrophage.
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PMID:Serum levels of neutrophil and eosinophil chemotactic activities in mastocytosis. 247 24

A diagrammatic representation of the interactions between mediators of hypersensitivity and leukocytes in early, late-phase, and ongoing asthma is shown in Figure 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 nonimmunologic (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 (M phi). 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 IFN-gamma, respectively. Macrophage-derived tumor necrosis factor (TNF) also amplifies the inflammatory response by its capacity to enhance eosinophil cytotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inflammatory cells in bronchial asthma. 270 38

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

In order to determine mast cell involvement in aspirin-induced bronchoconstriction, 16 aspirin-sensitive asthmatics and 18 control patients were studied for serum neutrophil chemotactic activity, using Nelsons method, before and after oral aspirin administration. A significant increase in NCA was observed in 6 aspirin-sensitive asthmatics during aspirin bronchoconstriction. In two persons the increase was lower. In the remaining 8 persons, no increase in NCA was observed during aspirin bronchoconstriction. None of the control patients exhibited an increase in NCA. The authors assume that, in some of the patients with aspirin-induced bronchoconstriction mast cells are really involved.
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PMID:Serum neutrophil chemotactic activity (NCA) during aspirin-induced bronchoconstriction. 329 81

There is now very substantial evidence to implicate mediators in the pathogenesis of asthma during both the early- and late-phase response. It seems likely that mast cells are activated since histamine was detected in early- and late-phase allergen- and exercise-induced asthma. On the other hand, the origin of NCA is still in some doubt, and the possibility exists that it may be derived from other cell types. Furthermore, there is no firm evidence that the mast cell is directly involved in pathogenesis and some evidence that it may have a secondary or amplifying role. There is an urgent need for further details of other mast-cell-associated mediators such as prostaglandins and leukotrienes. Measurements in the blood have the obvious disadvantage of only indirectly reflecting events in the lung. It seems likely that more invasive procedures such as fiberoptic bronchoscopy will yield more critical information regarding mast cells and their mediators in early- and late-phase reactions, as well as the effects of selective drugs and the role of other cell types.
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PMID:Provoked asthma and mast cells. 355 94

In order to evaluate the relationship between allergen-induced heat-stable neutrophil chemotactic activity (HS-NCA) release during early asthmatic reaction (EAR) and the presence of a late asthmatic reaction (LAR), serum HS-NCA was measured at three serum dilutions (1:5, 1:40, 1:200) during EAR induced by allergen in 26 atopic asthmatics, 13 with isolated EAR and 13 with EAR followed by LAR. HS-NCA was measured using a 48-well microchamber with 5-micron-pore-size nitrocellulose filters, using isolated neutrophils from healthy donors and the leading front technique. Subjects with LAR developed EAR after inhalation of a lower dose of allergen than subjects with isolated EAR. Increase in serum HS-NCA during EAR was significantly higher in subjects with isolated EAR than in subjects with EAR plus LAR at the 1:5 dilution, while it was significantly higher in subjects with EAR plus LAR than in the subjects with isolated EAR at the 1:200 dilution; the 1:40 dilution gave similar results in both groups. Changes in serum HS-NCA during EAR significantly correlated with the maximum decrease in forced expiratory volume in 1 s (FEV1) during LAR: a higher decrease in FEV1 during LAR was associated with a lower increase in HS-NCA at the 1:5 dilution (Spearman's rho = 0.43, rho = 0.03), and with a higher increase in NCA at the 1:200 dilution (Spearman's p = -0.46, p = 0.02). These results can be explained by the 'high-dose-inhibition' phenomenon. Assuming that HS-NCA is associated with mast cell degranulation in the airways after allergen challenge, these findings demonstrate that higher mast cell activation during EAR is present in subjects with a subsequent LAR than in subjects with isolated EAR.
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PMID:Relationship between serum heat-stable neutrophil chemotactic activity during early airway reaction to allergen and the pattern of airway response (early versus late reactions) in asthmatic subjects. 925 64