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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The bridging of IgE receptors on rat basophilic leukemia cells (RBL-2H3) results in a number of biochemical events that accompany histamine secretion. Prominent among these is the release of arachidonic acid from cellular phospholipids, which could be due to the activation of phospholipase enzymes. In the present experiments we studied the intracellular activation of phospholipase A2 (PLA2) during histamine release. RBL-2H3 cells were stimulated through the IgE receptor, and the homogenates were prepared and tested for phospholipase A2 activity on 1-stearoyl-2-[14C]arachidonyl-sn-3-phosphatidylcholine. The amount of activity in the homogenates was dependent on the concentration of secretagogue used to activate the cells. Under optimal conditions there was a 1.86 +/- 0.12-fold (mean +/- SEM, N = 44) increase in the activity found in homogenates of stimulated cells. Activity was present in homogenates prepared 30 sec after cell activation, was optimal between 5 and 10 min, and decreased later. In time course experiments the PLA2 activation preceded histamine release. The activation of the enzyme in the cell occurred in the presence of 10 microM EGTA in the extracellular medium, which completely inhibited release of arachidonic acid and histamine. However, the activity of the enzyme required Ca2+. The PLA2 activity in the homogenates and the extent of cell stimulation for histamine release were maximal at the same concentration of antigen, and both were blocked by the addition of a monovalent hapten. The enzyme in the homogenates was capable of cleaving arachidonic acid from different phospholipids. The production of lysophospholipids could play a critical role in histamine release from cells. These results demonstrate the activation of PLA2 enzyme in cellular homogenates during the secretory process.
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PMID:Phospholipase A2 stimulation during cell secretion in rat basophilic leukemia cells. 241 21

An association between the release of histamine and chondroitin sulfate E proteoglycan (PG) was demonstrated in human colonic mucosa (HCM). Colonic biopsy samples incorporated [35S]sulfate (2.7 X 10(6) +/- 188 X 10(3) cpm/mg of wet tissue; mean +/- SEM, n = 5) into PG, which was partially released into the culture medium during the incubation period. Ascending thin-layer chromatography of the released 35S-labeled PG after its digestion by chondroitin ABC lyase (chondroitinase, EC 4.2.2.4) followed by autoradiography yielded three products that migrated in the position of monosulfated disaccharides of N-acetylgalactosamine 4-sulfate and N-acetylgalactosamine 6-sulfate and of an oversulfated disaccharide possessing N-acetylgalactosamine 4,6-disulfate. Cultured colonic mucosa released 23.6 +/- 3.7 ng of histamine per mg of wet tissue (mean +/- SEM, n = 16) without any specific trigger. Comparison by linear regression analysis of the release of histamine and chondroitin [35S]sulfate E PG revealed a correlation coefficient (r) of 0.7 (n = 16; P less than 0.005). Histological examination of the colonic biopsies revealed the presence of many mast cells in various degrees of degranulation in the mucosa and submucosa, most of which were found in the submucosa. Incubation of the HCM biopsies in the presence of anti-human IgE revealed 58% +/- 12% (mean +/- SEM, n = 3) enhancement in the release of chondroitin [35S]sulfate E PG and 64% +/- 10% (mean +/- SEM, n = 4) of histamine release. The above correlation, the observation that most of the mast cells showed various degrees of degranulation, and the lack of heparin synthesis as opposed to the synthesis and immunological release of chondroitin sulfate E strongly suggest that the E mast cell exists in the human colon.
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PMID:Histamine and chondroitin sulfate E proteoglycan released by cultured human colonic mucosa: indication for possible presence of E mast cells. 241 44

The responses of human cutaneous, pulmonary, intestinal, and cardiac tissue mast cells to the histamine-releasing agent morphine sulfate (MS) were investigated in vitro. Human cutaneous mast cells released significant amounts of histamine in the presence of 1 to 100 mumol/L concentrations of MS. Histamine release was detectable within 5 minutes after challenge and was complete by 15 minutes. A maximal histamine release of 21.6% (+/- 1.4 SEM) was observed after stimulation with 100 mumol/L of MS. This MS effect was inhibited by the opiate receptor antagonist naloxone with a 59% inhibition detected at equimolar concentrations and an 88% inhibition occurring in the presence of a tenfold molar excess of naloxone. Naloxone did not alter the cutaneous mast cell response to the calcium ionophore A23187. Human mast cells derived from pulmonary, intestinal, and cardiac tissues, as well as blood basophils, did not release histamine after stimulation with 1 to 200 mumol/L of MS, whereas each of these cell preparations responded to an IgE-mediated stimulus. The results of this study demonstrate that cutaneous mast cells release inflammatory mediators after stimulation by MS, whereas mast cells residing in lung, heart, and gastrointestinal tissues do not. These observations indicate that human mast cells in different anatomic sites can vary in their functional responses.
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PMID:Functional heterogeneity of human mast cells from different anatomic sites: in vitro responses to morphine sulfate. 243 77

Accumulating evidence suggests a link between immediate hypersensitivity and cellular immunity. In this study, we examined the effect of interleukin 2 (IL-2) on basophil histamine release. Histamine-releasing activity of IL-2 was very weak with % histamine release of 2.9 +/- 1.3 (mean +/- SEM, n = 9) at 1:12 dilution. IL-2 at 1:1200 dilution slightly inhibited anti-IgE-induced histamine release by 22.4 +/- 18.6% (P greater than 0.05). There was a significant potentiation of release at 1:12 dilution of IL-2 with % enhancement of 78.7 +/- 42.2 (P less than 0.05). IL-2 enhanced the calcium ionophore A23187-induced histamine release in a dose-dependent fashion. IL-2 at 1:12 dilution significantly potentiated release by 28.8 +/- 6.3% (P less than 0.05). There was a slight suppression of formyl-methionyl-leucyl-phenylalanine (FMLP)-induced histamine release at 1:1200 dilution with % inhibition of 23.4 +/- 7.4 (P greater than 0.05). At 1:12 dilution, IL-2 significantly potentiated FMLP-induced release by 73.7 +/- 41.6% (P less than 0.05). Recombinant IL-2 (RIL-2) augmented anti-IgE-induced histamine release with a significant enhancement at 200 units/ml. Conventional IL-2 was more potent than RIL-2 in enhancing release. These results indicate that IL-2 enhances basophil histamine release and some part of the effect of IL-2 on basophils is derived from other factors contained in conventional IL-2.
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PMID:Effect of interleukin 2 on basophil histamine release. 243 59

The present study was undertaken to evaluate the effect of fenoterol, a selective beta 2-adrenergic agonist, on basophil histamine release. Fenoterol at 10(-7) to 10(-3) M did not inhibit the release of histamine induced by Dermatophagoides farinae extract (D.f.) from leukocytes from allergic patients sensitive to mite. Similarly, there was no suppression of histamine release induced by anti-IgE and formyl-methionyl-leucyl-phenylalanine under the influence of fenoterol. Fenoterol caused a slight inhibition of the calcium ionophore A23187-induced histamine release at 10(-3) M with % inhibition of 11.8 +/- 2.4 (means +/- SEM, P less than 0.05). There was no synergism between fenoterol and theophylline in inhibiting D.f.-induced histamine release. Fenoterol did not suppress the release of histamine induced by antigen at low as well as high levels of release. Based on the data on the effect of fenoterol on IgE-mediated histamine release, it was concluded that in contrast to a human lung mast cell system, the beta-adrenergic receptor-adenylate cyclase system is not a control mechanism in IgE-mediated basophil histamine release.
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PMID:Fenoterol, a selective beta 2-adrenergic agonist, and inhibition of IgE-mediated basophil histamine release. 244 20

We examined the effect of low density lipoprotein (LDL) on histamine release from purified human lung mast cells. LDL inhibited anti-IgE- induced histamine release in a dose-dependent manner, with 100 micrograms/ml LDL-protein inhibiting histamine release by 53 +/- 8% (mean +/- SEM); half-maximal inhibition occurred at 40-80 micrograms/ml. LDL also inhibited calcium ionophore A23187-induced histamine release in a dose-dependent manner, with 1 mg/ml of LDL inhibiting histamine release by 83 +/- 9%; half maximal inhibition occurred at 220-280 micrograms/ml. Inhibition by LDL was time-dependent: half-maximal inhibition of anti-IgE- induced histamine release by LDL occurred at 30-50 minutes of incubation. The inhibitory effect of LDL was independent of buffer calcium concentrations (0-5 mM) or temperature (0-37 degrees C). These data are consistent with a newly defined immunoregulatory role for LDL.
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PMID:Low density lipoprotein (LDL) inhibits histamine release from human mast cells. 244

The ability of purified anaphylatoxins to induce human lung mast cell mediator release was investigated. In eight anti-IgE responsive (histamine release = 22 +/- 5%, mean +/- SEM) mast cell preparations of 1-96% purity, C5a and C5a des Arg (0.55 pg/ml to 55 micrograms/ml), failed to elicit or potentiate histamine release; lung fragments were similarly unresponsive. The related peptide C3a was also inactive. All anaphylatoxins failed to induce mast cell leukotriene C4 (LTC4) and prostaglandin D2 (PGD2) release. LTC4 release was also negligible from basophils where C5a was a potent histamine release stimulus. Supernatants from C5a-challenged mast cells remained fully active on basophils, excluding carboxypeptidase inactivation of C5a as an explanation for the lung mast cell results. In contrast to lung, skin mast cells were C5a-responsive (histamine release = 8 +/- 1%, at 55 micrograms/ml, n = 2). We conclude that C5a, though devoid of activity on the human lung mast cell, is a human basophil and skin mast cell secretagogue. These findings demonstrate significant organ-specific heterogeneity in mast cell responsiveness.
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PMID:Differential effects of the complement peptides, C5a and C5a des Arg on human basophil and lung mast cell histamine release. 244 62

Human peripheral blood monocytes generated activities during 24-h culture that were capable of triggering histamine release from 17 of 18 human basophil donors. Monocytes and their in vitro transformed macrophages continued to elaborate these basophil histamine-releasing activities for at least 3 wk in culture. In the 18 basophil donors tested, maximum histamine release induced by monocyte supernatants was 33.8 +/- 5.9% (mean +/- SEM) of total basophil histamine content; optimum anti-IgE-induced release was 38.8 +/- 6.2%. Basophil histamine release in response to monocyte activities was optimal at 37 degrees C and at calcium concentrations of 2 to 5 mM. Release was greater than 90% complete 1 min after challenge and was inhibited by anti-allergic drugs. The mechanism of release appeared to be independent of IgE binding. Gel filtration of supernatants derived from both day 1 (monocyte stage) and day 14 (macrophage stage) cultures demonstrated activity peaks with approximate m.w. of 12,000 and 30,000. In contrast to the marked responsiveness of basophils, only 2 of 10 human lung mast cell preparations responded; release in those preparations was low: 3% and 13% histamine release, respectively. Thus, monocytes produce potent histamine-releasing activities with differential actions on basophils and mast cells.
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PMID:Human monocytes generate basophil histamine-releasing activities. 245 Sep 19

Suspensions of enzymatically dispersed human lung parenchymal mast cells were fractionated according to density by flotation through discontinuous Percoll gradients and examined for their responsiveness to release stimulants and pharmacologic agonists. Mast cells localized to all six density fractions (I-VI) examined: densities varied from specific gravities of 1.053 gm/ml to 1.123 gm/ml. Most (67%) lung mast cells localized to fractions III and IV, corresponding to specific gravities of 1.077 to 1.088 gm/ml, respectively. Histamine content increased with density from 2.7 +/- 0.3 pg per cell in fraction 1 to 4.8 +/- 0.7 pg per cell in fraction VI (mean +/- SEM; n = 19). Fraction III was least responsive to high concentrations of anti-IgE than to any other fractions and, along with fraction IV, the most responsive to ionophore A23187. All fractions released the arachidonate mediators prostaglandin D2 and leukotriene C4 in response to anti-IgE. In four of eight lungs tested, formyl methionine peptide (10(-6) to 10(-4) mol/L) weakly elicited histamine release (3% to 6%) in fractions I and II cells. Compound 48/80 (0.1 to 10 micrograms/ml; n = 3) failed to induce histamine release in any fractions. The cyclic adenosine monophosphate-active drugs, isoproterenol (10(-4) mol/L), dibutyryl cyclic adenosine monophosphate (3 mmol/L), and isobutylmethylxanthine (3 X 10(-4) mol/L) inhibited anti-IgE-induced histamine release from all fractions equivalently. Dimaprit (3 X 10(-5) mol/L) and cromolyn sodium (10(-5) -3 x 10(-3) mol/L) failed to significantly inhibit any fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Density heterogeneity of human lung mast cells. 245 45

Human synovium obtained at arthroplasty from patients with rheumatoid arthritis (RA) and osteoarthritis (OA) were characterized by assessing mast cell morphology, content and function. Histological studies confirmed significant numbers of mast cells in both RA and OA synovium. Electron microscopic data support the morphologic similarity between human synovial mast cells and human mast cells in lung and intestine. Likewise, synovial mast cells do not appear to be functionally different from pulmonary or intestinal mucosal mast cells. Mast cell suspensions with a cellular histamine content of 4.3 +/- 0.5 pg/cell (mean +/- SEM) released histamine following provocation with anti-IgE and calcium ionophore but not compound 48/80, f-met peptide or bradykinin. Prostaglandin D2 (PGD2) and leukotriene C4 (LTC4) were also released in response to anti-IgE. Auranofin inhibited anti-IgE provoked histamine, PGD2 and LTC4 release while gold sodium thiomalate, cromolyn and indomethacin had no effect on histamine release. Theophylline inhibited anti-IgE induced histamine release only at concentrations greater than or equal to 10(-3) M. Our study argues against functional or morphologic mast cell heterogeneity of human intestinal, lung and synovial origin and suggests that mast cells may have a pathogenic role in both RA and OA.
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PMID:Characterization of human synovial mast cells. 246 48


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