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 primary amine analog of compound 48/80 (nor-48/80) was purified and attached to Sepharose beads through an albumin link. Suspensions of rat peritoneal cells were passed over the beads in an affinity chromatography column, and the proportion of the mast cells that was retained by the beads was determined. Sixty-seven percent of the mast cells were found to be retained by the column, indicating the existence of a binding site for nor-48/80 on the exterior of mast cells. The beads were larger than the cells, and hence precluded the entry of the nor-48/80 into the cells. Neither the Sepharose beads nor the albumin link was responsible for this amount of binding because control beads without nor-48-80 retained only 22% of the mast cells. Mast cells incubated with large quantities of the beads in a batch procedure released up to 53% of the mast cell histamine, whereas control beads without the polymer released only 18%. This release could not be attributable to soluble nor-48/80 because only trace amounts of radioactive nor-48/80 were released from beads soaked overnight, and these supernatants released insignificant amounts of histamine when incubated with mast cells. These studies indicate the presence of a receptor for 48/80 on the mast cell membrane which can trigger histamine release.
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PMID:The site of action of the histamine releaser compound 45/80 in causing mast cell degranulation. 6 7

Pyridoxine, one of the B vitamins, has been shown to be useful in the treatment of childhood bronchial asthma by Collip et al. (1975). A double-blind study with 76 asthmatic children followed for five months indicated significant improvement in asthma following pyridoxine therapy (200 mg daily) and a reduction in dosage of bronchodilators and cortisone. Other reports have shown that nicotinamide, another B vitamin shows inhibitory activity in rat mast cell degranulation and histamine release (Bekier et al. 1974, Wiczolkowska and Maslinski, 1975, 1976). These results induced us to investigate if pyridoxine, like nicotinamide or disodium cromoglycate, exhibits pharmacological inhibitory activity in rat mast cell degranulation and histamine release induced by antigen or other non-immunological stimulants. We found that pyridoxine at concentrations of 10 (-3) M, or greater significantly inhibited rat mast cell degranulation and histamine release induced by phospholipase A, compound 48/80, antigen (egg albumin) or a mixture of dextran and phosphatidyl serine, respectively. In these experimental models, pyridoxine shows a pharmacological profile similar to nicotinamide and disodium cromoglycate, although weaker than the latter. In spite of this, the lack of toxicity of this vitamin at relatively high doses (1 or 1.5 g), the possibility that other mechanisms of action may be involved, such as the improvement in tryptophan metabolism reported by Collip following pyridoxine therapy, suggest that this vitamine merits additional research.
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PMID:[Effect of pyridoxine on histamine liberation and degranulation of rat mast cells]. 9 42

Agarose gel electrophoresis (at pH 8.6) was used for qualitative determination of pancreatic enzymes in duodenal juice. The various enzymes were identified by staining techniques with specific chromogenic substrates, by quantitative determination of enzymes in eluates of gel slices, and by immunoelectrophoresis. The various protein bands corresponded to the following enzymes (from the anode to the cathode): chymotrypsin, trypsin, carboxypeptidase A, chymotrypsin, amylase (around the slit), lipase, elastase, and trypsin. The method was applied to a study of exocrine pancreatic function in 10 adults and 83 children suspected of having malabsorption. The duodenal juice, also analyzed for trypsin and amylase content, was collected in fasting condition and after a test meal of water. In patients with normal pancreatic function, all the enzyme bands were present and easy to recognize. In 87 patients carboxypeptidase A was present as two bands in 68 (80%), anodal trypsin as two bands in 39 (45%), and cathodal trypsin as two bands in 85 (97%). Electrophoresis of duodenal juice gave as much information from the fasting sample as after the test meal. Six children with pancreatic insufficiency (cystic fibrosis and Shwachmar's syndrome) had no or only faintly stained enzyme bands and a strongly stained albumin-containing band most anodally. The method is simple, rapid, and useful in routine work. The combination of this qualitative test with a quantitative one (e.g. trypsin determination) provides good information about exocrine pancreatic function.
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PMID:Agarose gel electrophoresis of duodenal juice in normal condition and in children with malabsorption. 43 37

Our experiments have provided additional data in support of the concept that different mast cell activators follow distinct biochemical path-ways in the initiation of secretion and degranulation. To do this we have taken advantage of the observation that some serum proteins, and albumins in particular, have the capacity to inhibit selectively the release of amines from rat peritoneal mast cells initiated by some, but not all, stimuli. We show that the relative inhibition of release obtained is independent of the concentration of activator but dependent upon the concentration of albumin, indicating that the inhibitory process does not involve a direct activator--inhibitor interaction. Finally, our data demonstrate that the inhibition does not interfere with the ability of the acitivator to interact with the mast cell. Thus, cells incubated with activator in the presence of inhibitor become increasingly unresponsive, or desensitized, to subsequent challenge with activator in the absence of inhibitor. These combined data therefore provide evidence, that, in addition to a selectivity in the activation/desensitization process initiated by different mast cell stimuli, at least one of the biochemical steps subsequent to the activation step is also not shared by all mast cell stimuli.
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PMID:Two distinct mechanisms for the initiation of mast cell degranulation. II. A specific inhibition of amine release by serum proteins. 68 Sep 51

The various peptidases secreted by such exocrine tissues as gastric mucosa, pancreas and prostate are usually determined by catalytic methods. Another approach utilizes immunoassay. Endopeptidases were formerly assayed with protein substrates such as hemoglobin and albumin. These techniques are increasingly replaced by more specific ones using artificial peptide derivatives as substrates, some of which allow an increase in absorbance or fluorescence to be continuously recorded. The presently available methods of assaying pepsin, pancreatic trypsin, trypsinogen and carboxypeptidase A, enterokinase and several peptidases of human sperm are reviewed.
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PMID:The assay of exocrinous peptidases in clinical chemistry. 77 94

Infection of CFW mice with Trichinella spiralis induced a state of relative unresponsiveness to passive cutaneous anaphylaxis (PCA) induced with hen egg albumin and its corresponding antibodies. The unresponsiveness was to PCA produced either with immunoglobulin G1 (IgG1) or IgE type of antibodies, but was more pronounced with the latter. As few as 25 larvae given by stomach tube 20 days before induced this resistance, although 400 larvae induced a greater resistance. When 400 to 600 larvae were fed to mice, the refractoriness of these mice to PCA was noticed 15 days later. The sera of infected mice had the ability to inhibit mainly PCA induced by IgE. This inhibitory property of sera from infected mice was more pronounced 35 days after infection than 10 months later, when only weak inhibitory activity was detected. Purified rat IgE inhibited the PCA reactions induced in both mice and rats with mouse IgE-type antibody. At high concentrations, evidence of inhibition of the IgG1-induced PCA in mice was also obtained. We believe that the relative unresponsiveness of infected mice is due to an increase in production of IgE which competitively blocks the mast cell sites for other IgE molecules.
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PMID:Effect of Trichinella spiralis infection on passive cutaneous anaphylaxis in mice. 83 10

The study was undertaken to examine the effect of isoprinosine treatment on in vitro histamine release from peritoneal mast cells. The experiments were done on mice which received isoprinosine orally, at a dose of 50 or 100 mg per kilogram of body weight per day, in divided doses, every 8 hours, for a period of 1-9 days. After isoprinosine treatment, there was a significant decrease of in vitro Con A-induced histamine release from mast cells. This inhibitory effect was observed in both tested groups. In the second experiment, with mice sensitized with egg albumin, the treatment with isoprinosine gave also a significant inhibition of anaphylactic histamine release from mast cells, as compared with that of control without isoprinosine treatment. Results of both experiments suggested that isoprinosine may have some inhibitory effect on mast cell activation.
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PMID:The effect of isoprinosine treatment on histamine release from murine peritoneal mast cells. 128 65

Sixteen patients with allergic rhinitis were recruited into a double-blind crossover protocol studying the immediate effect of nedocromil sodium (NS) on the pattern of nasal symptoms and secretions after allergen challenge. After pretreatment with placebo or NS, allergen challenge resulted in pruritus, rhinorrhea, nasal congestion, and/or sneezing within 10 minutes in 12 of 16 subjects. Prostaglandin D2 (PGD2), a marker of mast cell degranulation, increased proportionately with symptom scores, remaining above the 95% confidence interval for 120 minutes after both pretreatments. No difference in PGD2 between the NS-treatment and placebo-treatment days was observed. Protein markers extravasated through the vasculature (albumin and IgG) or secreted by mucosal glands (lactoferrin) were assayed. Total protein, albumin, IgG, and lactoferrin all remained greater than 95% confidence interval for 100 minutes after allergen challenge in the placebo-pretreated group and 120 minutes in the NS-pretreated group. Although there appeared to be a trend for lower secretion of PGD2, albumin, and IgG in the NS-treated group, the overall differences did not achieve statistical significance. This protocol revealed that two topical 130 microliter doses of a 1% solution of NS failed to significantly reduce allergen-induced symptoms, PGD2 generation, or secretion of albumin, IgG, or lactoferrin when NS was compared with placebo. The anti-inflammatory and mast cell-stabilizing effects of NS may require more prolonged pretreatment before provocation to be effective.
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PMID:Effects of nedocromil sodium on allergen-induced rhinitis in humans. 131 Oct 8

We investigated the effects of unilateral electrical trigeminal ganglion stimulation (0.1 or 1.0 mA, 5 Hz, 5 ms, 5 min) on the morphology of blood vessels within the rat dura mater and tongue using light and transmission electron microscopy. Stimulation at both intensities caused changes which were confined to the ipsilateral post-capillary venules except in the tongue where arterioles were affected as well. Changes were more marked after 1.0 mA. Dramatic increases in the numbers of endothelial pinocytotic vesicles were found along the luminal and abluminal surfaces ipsilateral to the stimulation. Tight junctions remained largely intact, except that injected ferritin particles were occasionally trapped inside these junctions. Cytoplasmic microvilli and endothelial blebs were sometimes present as well. Approximately 80% of the examined dural post-capillary venules showed one or more of these endothelial changes. Horseradish peroxidase injected intravenously 5 min prior to stimulation was detected in the extracellular space surrounding dural blood vessels and within pinocytotic vesicles. Ferritin injected similarly, was also localized in post-capillary venule walls, interstitial spaces, intraendothelial vesicles and in vacuoles. Platelet accumulation and aggregation were present in approximately 10% of post-capillary venules in dura and tongue. These changes were associated with mast cell secretion, but neither vascular nor mast cell activation was observed in adult rats in whom C-fibers were destroyed during the neonatal period with capsaicin. The present observations provide morphological evidence which supports findings from previously reported albumin tracer studies suggesting enhanced transport and endothelial activation following electrical stimulation of small caliber afferent fibers.
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PMID:Ultrastructural evidence for neurogenically mediated changes in blood vessels of the rat dura mater and tongue following antidromic trigeminal stimulation. 137 61

Incubation of bovine serum albumin (BSA), rat serum albumin or rat plasma with medium conditioned by endotoxin stimulated rat peritoneal macrophages produced an activity that released histamine from isolated rat serosal mast cells. The amount of histamine-releasing activity (HRA) produced increased with the length of the incubation period, with the concentration of albumin, with the number of macrophages stimulated, and with the duration of exposure of the macrophages to endotoxin. Moreover, the formation of the HRA showed a dependency on the pH of the incubation medium with an optimum at pH 4.5. Boiling the medium conditioned by stimulated macrophages before its incubation with albumin or including the acid protease inhibitor, pepstatin with the conditioned medium prevented the formation of HRA. The generation of HRA was not inhibited by pretreatment of the macrophages with the inhibitor of protein synthesis, cycloheximide. Media from macrophages not stimulated with endotoxin failed to generate HRA. Histamine release from mast cells in response to the HRA was inhibited by pretreatment of the cells with antimycin A and deoxyglucose or by preincubation in Ca-free Locke's solution containing a calcium chelating agent. When injected intradermally into anesthetized Evan's Blue treated rats, the generated HRA produced a change in vascular permeability that was prevented by the H1 antagonist, diphenhydramine. Treatment of the HRA with carboxypeptidase A reduced its ability to stimulate histamine release from mast cells. Histamine-Releasing Peptide (HRP), a neurotensin-related octapeptide, shown previously by us to be formed by the action of cathepsin D or pepsin on albumin, was identified by radioimmunoassay in acid:acetone extracts of the histamine-releasing activity. It is concluded that the formation of HRA is due to the actions of enzymes released from macrophages acting on albumin. It is suggested that such histamine-releasing activity could be formed during the later stages of the inflammatory response and that HRP is one of the peptides present.
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PMID:Formation of histamine-releasing activity from albumin by medium conditioned by endotoxin-stimulated rat peritoneal macrophages. 138 Jul 64


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