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 model of topically induced ocular anaphylaxis was developed. Male Sprague-Dawley rats were immunized by intraperitoneal injections of egg albumin (EA) and alum and topically challenged with EA. Application of EA induced clinical (conjunctival edema) and histologic (mast cell degranulation) signs of anaphylaxis, when the antigen was preceded by topical application of dithiothreitol (DTT), a mucolytic agent. Rats challenged by four EA applications did not differ significantly in clinical edema or mast cell degranulation from those challenged by one EA application at the same (0.1 M DTT) pretreatment level, but there was significantly greater histologically assessed edema in the eyes challenged four times.
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PMID:Topically induced ocular anaphylaxis in rats immunized with egg albumin. 373 14

We previously showed that rats sensitized to egg albumin (EA) respond in vivo intraluminal antigen-challenge with decreased net absorption of water and electrolytes and depletion of mucosal histamine. However, administration of anti-histamines did not prevent the transport abnormalities. The present in vitro studies examined the effect of histamine to alter net ion transport and the ability of diphenhydramine (DPH) and cimetidine (CIM) to block the responses to both histamine and antigen. Control rat jejunum was mounted in Ussing chambers and histamine was added to the serosal side either in the absence or presence of DPH or CIM. In control tissues histamine caused a transient increase in short-circuit current (Isc) in a dose-dependent manner between 10(-5) and 10(-4) M which was blocked by 10(-5) M DPH but was unaffected by CIM in concentrations up to 10(-4) M. There was no response to EA. Jejunum from sensitized rats exposed to EA demonstrated a biphasic Isc response: a rapid transient rise followed by a somewhat less elevated but sustained component. In tissues pre-treated with DPH the initial peak was unaffected but the sustained component was reduced. Our results indicate that H1-receptors mediated the effects of histamine in rat jejunal mucosa but that during intestinal anaphylaxis histamine is responsible for only a portion of the antigen-induced transport abnormalities. Our data also suggest that IgE-mediated reactions in the intestine may involve an interaction between mast cell mediators and enteric nerves.
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PMID:Rat jejunal mucosal response to histamine and anti-histamines in vitro. Comparison with antigen-induced changes during intestinal anaphylaxis. 379 74

1 Peptide 401, a potent mast cell degranulating factor from bee venom, substantially inhibited the oedema provoked by subplantar injection of carrageenin or intra-articular injection of turpentine in the rat. The ED(50) of 401 was c. 0.1 mg/kg. The anti-inflammatory effect was assessed by measurement of the increased (125)I-albumin content of an injected site in comparison with an uninjected contralateral site.2 Peptide 401 also suppressed the increased vascular permeability due to intradermal injection of various smooth muscle spasmogens (histamine, bradykinin, 5-hydroxytryptamine (5-HT), and prostaglandins).3 Other comparable mast cell degranulating agents (48/80 and melittin) showed little evidence of anti-inflammatory activity when tested at comparable dosage on turpentine arthritis and carrageenin oedema.4 The anti-inflammatory effects were not abolished by pretreatment with mepyramine and methysergide, which abolished the increased vascular permeability produced by local injection of 401.5 The anti-inflammatory action of 401 was not affected by regional denervation or pretreatment with phenoxybenzamine, and was reduced but not abolished by adrenalectomy.6 Measurement of skin temperature, fractional extraction of (86)Rb and blood flow in perfused mesentery gave no evidence that the anti-inflammatory action of 401 was due to reduced tissue perfusion.7 It is concluded that 401 may exert its anti-inflammatory action directly by making the vascular endothelium anergic to phlogistic stimuli.
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PMID:Anti-inflammatory property of 401 (MCD-peptide), a peptide from the venom of the bee Apis mellifera (L.). 415 80

1 The role of histamine H1- and H2-receptors in mediating the cutaneous inflammatory response produced by exogenous histamine and the release of endogenous histamine from mast cells has been investigated by a method which permits simultaneous, quantitative measurement of vasodilatation, vascular permeability and oedema formation. 2 Histamine and the selective H1-receptor agonist, 2-(2-aminoethyl) pyridine, both produced vasodilatation, increased vascular permeability and oedema formation whereas the selective H2-receptor agonist, dimaprit, produced only vasodilatation. 3 Mepyramine and cimetidine both reduced the vasodilatation response to histamine, the combination of antagonists being superior to either antagonist alone. Mepyramine (but not cimetidine) virtually abolished extravascular albumin accumulation and oedema formation. 4 Mepyramine and cimetidine both reduced the vasodilatation response produced by active cutaneous anaphylaxis and compound 48/80. However, mepyramine was less effective in reducing the vascular permeability response to mast cell degranulation than to histamine. 5 In conclusion, the vasodilator response to histamine is mediated by both H1- and H2-receptors; the permeability response to histamine is mediated solely by H1-receptors. A combination of H1- and H2-receptor antagonists appears to be more effective than either antagonist alone in reducing cutaneous inflammatory reactions involving histamine.
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PMID:Evaluation of the role of Histamine H1- and H2-receptors in cutaneous inflammation in the guinea-pig produced by histamine and mast cell degranulation. 610 40

Eosinophil peroxidase (EPO) at relatively low levels (4-30 mU), when supplemented with H2O2 and a halide, induced mast cell degranulation. Histamine release occurred without concomitant release of the cytoplasmic marker lactic dehydrogenase (LDH), and this, together with ultrastructural studies, indicated a noncytotoxic effect comparable with that induced by other mast cell secretagogues. At pH 7.4, iodide was effective at concentrations down to 10(-5) M, and although chloride alone was ineffective at 0.1 M, a combination of 0.1 M chloride and 10(-6) iodide could meet the halide requirement. Chloride alone was effective at pH 6.5 and 6.0. EPO could be replaced by myeloperoxidase. When the EPO level was increased to 100 mU, combination with H2O2- and iodide-induced cytotoxic histamine release as indicated by concomitant LDH release and ultrastructural evidence of cell disruption. This cytotoxic response reverted to a secretory one on the addition of albumin. Peroxidase was detected on the surface of extruded granules by diaminobenzidine cytochemistry. The mast cell granule (MCG)/EPO complex when supplemented with H2O2 and iodide was more effective than free EPO in the stimulation of mast cell secretion. The stimulation of mast cell mediator release by the EPO-H2O2-halide system and the formation of MCG/EPO complexes with augmented cytotoxic activity may influence the adjacent inflammatory response.
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PMID:Eosinophil peroxidase-induced mast cell secretion. 615 83

Somatostatin, in concentrations up to 100 ng/ml, had no effect on mast cell secretion induced either by compound 48/80 or by the ionophore A23187. In higher concentration somatostatin induced mast cell secretion. Light and electron microscopic observations showed that the secretory response was identical with that induced by 48/80 and involved extrusion of secretory granules by exocytosis. As with 48/80, this response to somatostatin was inhibited by treating the mast cells with EDTA or EGTA or by exposing them briefly to A23187 in calcium-free media, all of which procedures seemingly deplete cellular calcium stores. Reintroduction of calcium (but not magnesium), restored secretory responsiveness. Somatostatin-induced secretion further resembled that induced by 48/80 or A23187 in its intensity, rapid time course, and dependence on albumin. Pretreatment of mast cells with dibutyryl cyclic AMP or 8-bromo cyclic AMP substantially reduced the secretory responses to both somatostatin and 48/80 but had little effect on the response to A23187. Somatostatin, like 48/80, lowered intracellular cyclic AMP levels in a time and dose-dependent fashion. Finally, as earlier found for 48/80, somatostatin attached to Sepharose columns retarded the passage of mast cells and elicited histamine release indicating an action at the cell surface. The stimulant action of somatostatin is thus very similar to that of the classic mast-cell secretagogue compound 48/80.
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PMID:Somatostatin-induced histamine secretion in mast cells. Characterization of the effect. 616 54

Two vitamins, ascorbic acid (AA) and pyridoxine have been suggested by others as useful drugs for the treatment of bronchial asthma, although the views concerning AA or controversial. We have tested both vitamins in some models of histamine release and experimental anaphylaxis. AA does not inhibit mast cell degranulation induced by phospholipase A and histamine release from isolated rat mast cells induced by compound 48/80 or antigen (egg albumin). On the contrary, in the latter tests pyridoxine exerts inhibition in a range of concentrations from 10(-3)-10(-2) M. We conclude: 1. There is no experimental basis for considering ascorbic acid as a prophylactic antiasthmatic drug as is disodium cromoglycate. 2. Pyridoxine must receive additional basic and clinical investigations in this field.
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PMID:Ascorbic acid and pyridoxine in experimental anaphylaxis. 616 75

Effect of disodium cromoglycate (DSCG) on hemolysis of rat erythrocytes was studied. The heat-induced hemolysis was remarkably inhibited by DSCG. This effect was not affected by normal rat serum and was maintained for longer than 60 min similar to the activity in clinical use, although the inhibitory effect of DSCG on reagin-induced histamine release from mast cell disappeared rapidly in 5 min after administration. Non-steroidal anti-inflammatory drugs such as flufenamic acid or phenylbutazone which are known to inhibit the hemolysis depending on their protein stabilizing activities inhibited both of the heat-induced hemolysis and albumin denaturation, but DSCG did not inhibit the albumin denaturation. Furthermore, it was also observed that DSCG inhibited the hemolysis induced by lipophilic agents such as saponin, linoleic acid or phospholipase C. These findings suggest that DSCG has a certain membrane stabilizing activity, in addition to the inhibitory effect on reagin-induced histamine release, and that the activity may be probably related to membrane lipids rather than membrane-proteins.
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PMID:Stabilizing action of disodium cromoglycate on erythrocyte membrane. 617 79

The pharmacology of histamine-induced increases in microvascular permeability has been studied in rat skin. Histamine caused dose-dependent increases in microvascular permeability, assessed as increases in extravascular albumin accumulation. The responses to histamine were inhibited in a dose-dependent manner by pretreatment with mepyramine and were not changed by cimetidine. 2-(2-Aminoethyl)pyridine also increased microvascular permeability whereas impromidine did not. These results suggest that H1-receptors and not H2-receptors are involved in the permeability response to histamine in rat skin. In contrast, dimaprit increased microvascular permeability and responses to dimaprit exceeded the maximum response to histamine. The response to dimaprit proved to be independent of H2 receptors and was consistent with an indirect response due to mast cell degranulation.
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PMID:Studies on cutaneous vascular permeability in the rat: increases caused by histamine and histamine-like agents. 623 Sep 1

The accumulation of mast cells is characteristic of a number of pathological states. We demonstrate here the directional motility of mast cells in vitro in response to tumor-derived peptides. Rat peritoneal mast cells were isolated on Percoll gradients and maintained in serum-free medium containing transferrin, albumin, soybean lipid, and cholesterol. The isolated mast cells migrated under agarose in response to medium conditioned by any of eight tumor cell lines but not to medium conditioned by any of a variety of nontumorigenic cell types. The tumor-derived activity is dialyzable (cutoff, Mr 3500), stable to trypsin treatment and to heating at 56 degrees, but destroyed by heating to 100 degrees or by treatment with Streptomyces griseus protease or carboxypeptidase A. Ultrafiltration suggests a molecular weight of 300 to 1000. Two tripeptides, glycylhistidyllysine and N-formylmethionylleucylphenylalanine, were also found to be potent chemoattractants for mast cells. N-Formylmethionylphenylalanine and valylglycylserylglutamic acid (eosinophil chemotactic Factor A) had significantly less chemoattractant activity over the same range of concentrations. Several peptide analogues of glycylhistidyllysine were tested and found to have no activity. The growth of capillary blood vessels toward a growing tumor is generally preceded by an accumulation of mast cells at the tumor site. Based on the results presented here and previous data from our laboratory on mast cell stimulation of capillary endothelial cell migration, we propose an hypothesis that the chemoattraction of mast cells by tumor-derived peptides may be an important early event in tumor neovascularization.
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PMID:Stimulation of rat peritoneal mast cell migration by tumor-derived peptides. 664 May 37


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