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)

We have attempted to review the current state of our knowledge concerning the human basophilic leucocyte, drawing on experimental data derived from animals when necessary. Long neglected, a great deal has been learned about these cells in recent years, about their morphology, their biochemical constitutents and their ability to synthesize certain of these constitutents, their interactions with homocytotropic antibodies, their release of mediators in anaphylaxis, their response to chemotatic stimuli, their participation and progressive degranulation in cell-mediated hypersensitivity reactions, and their capacity for ingesting and releasing certain exogenous tracers. Despite this vast accumulation of new information, much more must be learned before we can confidently describe the role of basophils, or of the closely related mast cells, in health or disease. It seems most unlikely that either cell exists for the purpose of destroying the organism in anaphylactic shock. Nonetheless, it is highly probably that basophil/mast cell function is closely related to the potent chemicals stored within their cytoplasmic granules. One likely possibility holds that small amounts of these chemicals are required for homeostasis (e.g., for regulation of the tone of the microvasculature) and that these cells function by releasing such substances continuously, as they are needed, in small aliquots rather than by explosive discharge. This hypothesis requires that basophils be capable of releasing their contents in piecemeal fashion. Such gradual release apparently occurs in delayed-type hypersensitivity reactions, but the mechanisms responsible for this form of degranulation have not yet been identified. This hypothesis also requires that physiological, rather than pharmacological, roles be found for histamine, heparin and possibly for other components of the basophils/mast cell granules. Progress in this direction has been extremely slow.
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PMID:Basophilic leucocytes: structure, function and role in disease. 5 13

In the presence of L-cysteine, a selective and marked enhancement of the in vitro, immunologic release of slow reacting substance of anaphylaxis (SRS-A) from human peripheral leukocytes, sensitized monkey lung fragments, and sensitized guinea pig lung fragments was observed. In the rat, cysteine, but not sodium sulfide, enhanced the calcium ionophore (A23187)- induced release of SRS-A in vitro from mixed rat peritoneal cells and in vivo from the rat peritoneal cavity. Pretreatment of rats with cysteine also enhanced the IgGa-and anti-rat IgE-mediated release of SRS-A in vivo in the rat. These studies indicate a common biochemical mechanism involved in the formation and release of SRS-A from these different tissues and cells and further confirm the observation that the rat mast cell is not a major source of SRS-A in the rat.
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PMID:The effect of thiols on the immunologic release of slow reacting substance of anaphylaxis. II. Other in vitro and in vivo models. 5 39

Patients with idiopathic acquired cold-induced urticaria were evaluated for the release of the preformed mast-cell mediators of immediate-type hypersensitivity during a study in which one arm was immersed in ice water while the other arm remained as a control. Blood specimens were obtained from each arm serially over a one-hour interval, and serum speciments were assessed for histamine, eosinophil chemotactic factor of anaphylaxis, and complement components. Levels of histamine and eosinophil chemotactic factor rose in the arm subjected to cold immersion for three minutes, with peak values occurring between two and five minutes and returning to base line by 30 minutes. No changes occurred in the control arm or in the immersed arm of normal subjects. Assessment of the classical and alternative complement pathways showed no abnormalities. This initial observation of release of eosinophil chemotactic factor of anaphylaxis in vivo along with histamine assigns the mast cell a central role in cold urticaria.
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PMID:Cold urticaria: release into the circulation of histamine and eosinophil chemotactic factor of anaphylaxis during cold challenge. 5 69

Peripheral blood leukocytes (PBL) and free respiratory cells (RC) of the mast cell-basophil type were obtained from normal rhesus monkeys or rhesus monkeys with defined immediate-type hypersensitivity to ascaris antigen (AA). PBL or RC from the latter were exposed to AA and the former were exposed to anti-IgE. Histamine (H) release and release of a slow reacting substance of anaphylaxis (SRS-A) occurred following exposure of the appropriate cells to AA or anti-IgE. The release of both H and SRS-A from PBL was potentiated by D2O. D2O did not potentiate release of SRS-A or H from RC due to anti-IgE to the same extent. Although potentiation of H release from RC due to AA was observed in the presence of D2O in some individual animals, this could not be demonstrated by statistical analysis of group results. We could not demonstrate potentiation of SRS-A release from RC due to anti-IgE or AA. The results suggest the possibility that there may be differences in antigen reactive cells of the respiratory tree and peripheral blood and biochemical studies may be of use in demonstrating these differences.
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PMID:IgE-mediated histamine and SRS-A release from respiratory cells and peripheral blood leukocytes of rhesus monkeys. 5 54

The capacity of Balb/c mice maintained since weaning on a 4% protein diet to express in vivo immediate (type 1) hypersensitivity reactions was compared to that of age-matched animals maintained on a normal (18%) protein diet. The deprived mice had a lower total cellular population and lower mast cell numbers in their peritoneal cavity. However, the mean cellular histamine content was comparable between the two groups. The skin responses of malnourished mice to the histamine liberator 48/80 were depressed but both groups reacted equally to passive cutaneous anaphylaxis when sensitized with serum from immunized mice. These studies indicate that protein deprivation has not inhibited the capacity to synthesize physiologically active amines or to impair the biochemical pathway of amine release from mast cells.
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PMID:Effect of a low protein diet on the capacity of mice to express a type I hypersensitivity response. 7 50

This review demonstrates that basophils reflect skin and lung mast cell reactivity and show characteristic changes in mediator release associated with clinical disease. Although the numbers of IgE molecules and IgE receptors on basophils have been enumerated, these have, in most instances, little influence on the release of histamine after challenge. There is, rather, a parameter of "releasability" that may be a major variable in allergic disease states. Basophils contain and release histamine, the eosinophil chemotactic factor of anaphylaxis (ECFA), a slow reacting substance of anaphylaxis (SRS-A), and a kallikrein. The release process is controlled by hormone-basophil receptor interactions that determine the cyclic AMP level; plasma and tissue adenosine levels appear prominent in this control. Histamine feeds back to negatively modulate basophil and mast cell release through a specific histamine 2-receptor; it also inhibits lymphocyte and neutrophil function. Like neutrophils, basophils contain beta-glucuronidase while neutrophils contain SRS-A and a low-molecular-weight ECF. The stimuli for primary basophil and neutrophil release are, however, quite different, although phagocytic stimuli, which fail to cause basophil mediator release, potentiate the IgE response. It is concluded that basophols play a significant in vivo role in inflammation by acting as an interface between foreign antigens, the serum cascade systems, and other inflammatory cells.
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PMID:The role of basophils in inflammatory reactions. 7 20

The net percentage of release of arylsulfatase activity from purified rat mast cells induced by rabbit anti-rat F(ab')2 was consistently only about 1/3 that of histamine. Isoelectric focusing of the released and residual arylsulfatase activities demonstrated specific release of the A type without B and a net percentage of immunologic release of arylsulfatase A equivalent to that of histamine. When the net percentage of histamine and arylsulfatase A release were nearly maximal (88 and 76%) in response to the calcium ionophore A23187, specific release of arylsulfatase B did not occur. Thus, arylsulfatase A and not B was associated with the secretory granule released from the rat mast cell by reversed anaphylaxis or the calcium ionophore. In contrast, subcellular fractionation of water-lysed mast cells yielded arylsulfatase B with the heparin- and chymase-containing granule fraction and arylsulfatase A in the aqueous fraction comprised of cell sap and granule water eluate. It may be that arylsulfatase B resides in a minor second granule, whereas arylsulfatase A is loosely associated with the predominant secretory granule of the rat mast cell.
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PMID:Release of arylsulfatase A but not B from rat mast cells by noncytolytic secretory stimuli. 8 Dec 31

IgE is a homocytotropic antibody which binds to the surface of the mast cell. Antigen with affinity for IgE triggers conformational change at the cell surface, resulting in the release of chemical mediators from the mast cell granules. The mediators histamine, slow reacting substance of anaphylaxis and eosinophil chemotactic factor cause smooth muscle contraction, increased capillary permeability, eosinophil attraction and increased glandular secretions. The release of mediators from the mast cell granules is controlled by intracellular levels of cyclic nucleotides. In particular, elevated cyclic AMP inhibits mediator release. Adrenergic, cholinergic and prostaglandin receptors all influence mediator release. The characteristic immunopathology of immediate hypersensitivity reactions is a result of local or systemic mediator release. Such reactions include anaphylaxis, asthma, allergic rhinitis, urticaria and angioedema. Similar immunopathology may sometimes result from mechanisms not involving IgE or histamine mediators. Routine investigation of patients with immediate hypersensitivity should include eosinophil counts and IgE levels in blood and secretions, and immediate hypersensitivity skin tests. RAST testing is not routine. Therapeutic principles of these reactions include restoration of inhibitory levels of cyclic nucleotides, antagonism of mediator effects and immunological manipulation of the IgE mediated allergic reaction.
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PMID:The immunological basis of immediate hypersensitivity. 8 47

p-Chlorophenylthiobutanol (W-2719) has been found to effectively inhibit immunologic and non-immunologic histamine release and mast cell degranulation. It has been found to effectively suppress passive cutaneous anaphylaxis (PCA) reaction not be antihistaminic action, but by inhibiting the release of allergic mediators.
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PMID:4-(p-Chlorophenylthio)butanol (W-2719), a new non-antihistaminic drug for immediate hypersensitivity allergies. 9 May 12

Previous work showed that anaphylaxis, mast cell population, and tissue histamine content are reduced in guinea pigs given DDT injections. This study was intended to determine whether dietary intake of DDT causes similar effects. Rats immunized with diphtheria toxoid and fed diets containing DDT at 20 and 200 ppm levels for 31 days did not show effects on their serum antitoxin titers, but the numbers of metachromatically stained, histamine-containing mast cells in mesenteries were reduced: in the 20 ppm group by 46% and in the 200 ppm group by 61%. The severity of anaphylactic shock was also reduced in proportion to the DDT dietary levels, and, thus, the magnitude of mast cells. Apparently, daily dietary DDT intake above 2.2 mg DDT/kg of body weight alters the physiology of mast cells in the rat, and thus affects histamine-mediated reactions.
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PMID:DDT and immunological responses. 3. Reduced anaphylaxis and mast cell population in rats fed DDT. 23 22


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