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 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

Since asthma has been recognized as a chronic inflammatory airway disease, inflammatory markers are useful tools to show the degree of allergic airway inflammation. Asthmatic airway is characterized with infiltration of activated Th2 lymphocyte, eosinophils and mast cells/basophils. Eosinophil derived proteins such as ECP, MBP and EDN are important markers indicating eosinophilic inflammation. Histamine and tryptase are the products of mast cell/basophil activation. These markers are detected in sputum, BALF, serum and urine, and increased in asthmatics. In addition to these markers, NO concentration in exhaled air, cytokines such as IL-4, IL-5, chemokines such as RANTES, eotaxin, LTE4, MMP are inflammatory markers to indicate the quality and quantity of asthmatic airway inflammation. Assessment of these markers, therefore, contributes to better control of asthmatic symptoms with appropriate therapy.
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PMID:[Airway inflammatory marker]. 1167 35

Bronchial asthma is a chronic disease of the respiratory tract. Search for alternative to presently used therapies seems to be the way to obtain a better control of asthma. Heparin is an acidic mucopolysaccharide and in the past years there has been a number of reports on the role of heparin and low-molecular-weight heparin (LMWH) in chronic inflammatory disorders of the respiratory tract. Our aim was to estimate the effect of long-time LMWH nebulization on selected parameters in asthmatic patients. Twenty-four patients entered the study. All of them were subjected to bronchoscopy with BAL, in 8 patients this procedure was performed twice: before and after heparin treatment. After 14 days of treatment we observed an increase in FEV1 (from 73.93 +/- 14.14% (in % of nominal value) to 89.62 +/- 10.08% (p = 0.0049). Additionally we noted a decrease in the percentage of eosinophils and lymphocytes in BAL sediments, from 4.86 +/- 3.48% to 1.25 +/- 2.76%; p = 0.0006 and from 5.39 +/- 2.25% to 2.94 +/- 1.23%; p = 0.0209, respectively. This changes were paralleled by a drop of EG2 in BAL supernatant from 1.00 +/- 0.99 to 0.13 +/- 0.35, p = 0.0256. In blood serum level of histamine 0.74 +/- 0.77 to 0.1 +/- 0.22; p = 0.0493. We did not observe significant changes in IL-5, sVCAM-1 or ECP concentrations in serum. Also different LMWH dosing (5-10 kUIC anti-Xa b.i.d.) did not produce any dose-response effect. We conclude, that LMWH in nebulization can be a valuable add-on treatment in bronchial asthma, and its most likely mechanisms of action are: prevention of mast cell degranulation (histamine decrease), decreased eosinophil activation (lower EG2), and modification of inflammatory cells influx (decreased percentages of eosinophils and lymphocytes in BAL).
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PMID:[Mechanisms of action of nebulized low molecular weights heparin in patients with bronchial asthma]. 1505 58