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PubMed1979

Cholinergic-mediated gastric mast cell degranulation with subsequent histamine H1-and H2-receptor activation in stress ulceration in rats.

The effects of atropine, mepyramine, metiamide or NaHCO3 on gastric ulceration, gastric secretion and gastric mast cell degranulation were studied in stressed pylorus-occluded rats. The influence of dexamethasone pretreatment on stress ulcers in animals without pylorus occlusion (intact rats) was also examined. Stress produced a high glandular lesion incidence and ulcer index, and markedly lowered gastric secretion and glandular wall mast cell counts. Injected 0.5 h before stress, atropine, mepyramine or metiamide strongly antagonised ulceration. Atropine or metiamide, but not mepyramine, reduced gastric secretion. Only atropine prevented stress-induced mast cell changes. NaHCO3, given intragastrically before stress, did not prevent ulceration or mast cell degranulation despite complete neutralisation of gastric acid. Dexamethasone-induced gastric mucosal mast cell depletion could reduce stress ulceration. The findings show that stress degranulates stomach mast cells via a cholinergic pathway; released histamine from this source is largely responsbile for gastric ulceration through H1- and H2-receptor effects. Histamine H2-receptor-mediated gastric acid may play only a small contributory role in stress ulcers in rats. The antiulcer mechanisms of histamine H1- and H2-receptor blockade are discussed.

Animals↗
PubMed1985

Amino acid sequence of bumblebee MCD peptide: a new mast cell degranulating peptide from the venom of the bumblebee Megabombus pennsylvanicus.

A new 28 amino acid peptide, we recently isolated from the venom of the bumblebee Megabombus pennsylvanicus. has been characterized. The peptide, Met-Cys-Ile-Cys-Lys-Asn-Gly-Lys-Pro-Leu-Pro-Gly-Phe-Ile-Gly-Lys-Ile-Cys- Arg-Lys-Ile-Cys-Met-Met-Gln-Gln-Thr-His(NH2), has been named bumblebee mast cell degranulating (MCD) peptide due to its ability to degranulate rat peritoneal mast cells, and its resemblance to the bee venom MCD peptide. Bumblebee MCD peptide, unlike bombolitins, the other mast cell degranulating heptadecapeptides of bumblebee venom, is not lytic and releases histamine at a dose as low as 0.05 micrograms/ml (1.6 X 10(-8) M).

Amino Acid Sequence↗
PubMed1993

Topical tiacrilast, a potent mast cell degranulation inhibitor, does not improve adult atopic eczema.

Tiacrilast is a potent mast cell degranulation inhibitor in vitro and in animal studies. Since mast cells and their mediators are possibly involved in atopic eczema, we have studied a topically applied 3% hydrogel formulation of tiacrilast against vehicle in a multicenter, double-blind, placebo-controlled trial. Drug or vehicle were applied on involved skin for 28 days. Efficacy was assessed weekly using a 4-point scale for erythema, scaling, induration, exudation and pruritus. An overall assessment of the sites for efficacy and site preference was performed at the end of treatment. In the 32 patients evaluable for efficacy, > 33% improvement was noted on 78% of the drug- and 75% of the vehicle-treated sites, with no statistically significant differences for any of the parameters tested. Treatment was generally well tolerated by all patients. These data suggest that mast cells may not play a major role in the maintenance of atopic eczema lesions.

Administration, Cutaneous↗
PubMed1996

Effects of in vitro mast cell degranulation on human lung beta-receptor binding parameters.

BACKGROUND: Numerous studies have demonstrated that subjects with allergic asthma have beta-adrenergic hyporesponsiveness, predisposing these individuals toward bronchospasm, mucous production, and mast cell degranulation. Since sympathetic innervation of the human respiratory tract is sparse, reduced beta-responsiveness probably results from alterations at or beyond the receptor level. OBJECTIVE: We therefore examined whether anaphylaxis of human lung tissue acutely modulated the human lung beta-receptor system in ways that might lead to decreased beta-adrenergic responsiveness. METHODS: Fresh thoracotomy peripheral lung samples from 26 patients were incubated with (anaphylaxis) or without (control) anti-IgE (1:100) for up to 90 minutes and histamine release was documented. Lung fragments were quick frozen at various times after anti-IgE for analyses of beta-receptor binding parameters. Antagonist Kd (dissociation constant) and receptor concentration values were determined using (-)[125I]pindolol and agonist IC50 values were determined using isoproterenol. RESULTS: In comparison with time O, neither anaphylaxis nor control samples had differences in receptor binding parameters with time. There were also no differences between anaphylaxis and control lung samples at any time point, and ratios of log control binding parameter/log anaphylaxis binding parameter ranged from 0.96 to 1.01. CONCLUSIONS: Anaphylaxis of lung does not lead to acute changes in antagonist or agonist affinity for beta-receptors or changes in receptor concentration. Under the conditions studied, lung mast cell degranulation does not acutely alter the human lung beta-receptor system in ways that might account for the beta-adrenergic hyporesponsiveness found in allergic asthma.

Adult↗
PubMed1999

Reciprocal effects of interleukin-4 and interferon-gamma on immunoglobulin E-mediated mast cell degranulation: a role for nitric oxide but not peroxynitrite or cyclic guanosine monophosphate.

We report that cultured rat peritoneal cells spontaneously synthesize nitric oxide and this is associated with active suppression of mast cell secretory function. Addition of interleukin-4 (IL-4) or the nitric oxide synthase inhibitor N-monomethyl-l-arginine to peritoneal cells inhibited nitric oxide synthesis and enhanced anti-IgE-mediated mast cell degranulation, measured as serotonin release. Interferon-gamma (IFN-gamma) completely overcame the enhancement of serotonin release and suppression of nitrite production induced by IL-4. Over several experiments, with or without IL-4 and/or IFN-gamma, serotonin release correlated inversely with nitrite production. On a cell-for-cell basis, non-mast cells produced approximately 30 times more nitrite than mast cells in peritoneal cell populations, with or without IFN-gamma stimulation. The nitric oxide donor S-nitrosoglutathione inhibited anti-IgE-induced serotonin release from purified mast cells, whereas 8-bromo-cyclic GMP, the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, superoxide dismutase and the peroxynitrite scavenger uric acid, were without effect. We conclude that IL-4 and IFN-gamma reciprocally regulate mast cell secretory responsiveness via control of nitric oxide synthesis by accessory cells; the nitric oxide effect on mast cells is direct but does not involve cyclic GMP or peroxynitrite.

Analysis of Variance↗
PubMed1997

Relationship between changes of active oxygen metabolism and blood flow and formation, progression, and recovery of lesions is gastric mucosa of rats with a single treatment of compound 48/80, a mast cell degranulator.

The relationship between the changes of active oxygen metabolism and blood flow and the formation, progression, and recovery of lesions was examined in the gastric mucosa of rats treated once with compound 48/80, a mast cell degranulator. Gastric mucosal lesions appeared 0.5 hr after compound 48/80 treatment, became worst at 3 hr, and recovered fairly well at 12 hr. Increases in gastric mucosal lipid peroxide content and xanthine oxidase and myeloperoxidase activities and decreases in gastric mucosal vitamin E and hexosamine contents and Se-dependent glutathione peroxidase activity occurred with the formation and progression of gastric mucosal lesions. These changes were attenuated with the recovery of the lesion. Gastric mucosal nonprotein SH content decreased with the formation of gastric mucosal lesions, and this decreased SH content returned to near the original level with lesion progression. No changes in gastric mucosal superoxide dismutase and catalase activities occurred with the formation, progression, and recovery of gastric mucosal lesions. Gastric mucosal blood flow decreased with the formation of gastric mucosal lesions, and this decreased blood flow recovered with lesion progression. Serum serotonin concentration, an index of mast cell degranulation, increased with the formation of gastric mucosal lesions, and this increased serotonin level was attenuated with lesion progression and recovery. Pretreatment with ketotifen, a connective tissue mast cell stabilizer, prevented the formation of gastric mucosal lesions, the increases of gastric mucosal lipid peroxide content, xanthine oxidase and myeloperoxidase activities, and serum serotonin level; and the decreases of gastric mucosal nonprotein SH content, glutathione peroxidase activity, and blood flow found at 0.5 hr after compound 48/80 treatment. These results indicate that the changes of gastric mucosal active oxygen metabolism and blood flow are closely related to the formation, progression, and recovery of gastric mucosal lesions in rats with a single compound 48/80 treatment. The present results also suggest that this compound 48/80-induced gastric mucosal injury could be a kind of ischemia-reperfusion-induced injury occurring through degranulation of connective tissue mast cells.

Animals↗
PubMedDate not supplied

Mast cell degranulation does not contribute to ischemic preconditioning in isolated rabbit hearts.

Preconditioning the heart with a short period of ischemia makes it resistant to infarction from a subsequent ischemic insult. We have proposed that preconditioning is triggered by the release of endogenous substances including adenosine which activate protein kinase C through receptormediated cell signaling pathways. However, it has also been proposed that the initial brief ischemia may result in mast cell degranulation without significant myocardial damage, making it less likely that the toxic granule contents could be released to irreversibly damage vulnerable myocardial cells during the subsequent prolonged ischemia. To study the role of mast cells in ischemic preconditioning (PC) isolated rabbit hearts were subjected to 30 min of regional ischemia followed by 120 min of reperfusion. Infarct size was measured with triphenyltetrazolium chloride. In control hearts infarction was 31.9 +/- 2.6% of the risk zone. Preconditioning with 5 min of global ischemia and 10 min of reperfusion reduced infarct size to 5.6 +/- 6.1% (p < 0.01). When disodium cromoglycate (DSCG)(10 microM), a mast cell stabilizer, was infused shortly before the long ischemia it did protect the heart (12.8 +/- 2.9% infarction, p < 0.01 vs control) which supports the mast cell theory. However, a mast cell degranulating agent, compound 48/80 (24 mg/L), added to the perfusate prior to the 30 min ischemic period could not mimic PC (39.7 +/- 5.6% infarction). Mast cell granules are rich in histamine, and the latter was assayed in myocardium by immunoassay as a marker of intact granules. In homogenized left ventricle from normal rabbit hearts and those following a standard PC protocol of 5-min global ischemia/10-min reperfusion, histamine contents were 9.3 +/- 1.4 and 8.9 +/- 1.4 ng/g wet tissue, respectively. Compound 48/80 reduced histamine levels to 2.9 +/- 0.6 ng/g (p < 0.05 vs control). Although baseline histamine contents were 10-fold higher in rats, PC also had no effect, but compound 48/80 reduced content by 91%. Therefore, histamine tissue content and presumably mast cell granules were unaffected by a PC protocol which successfully protected ischemic myocardium, while pharmacological myocardial histamine depletion was not associated with protection. Hence, mast cells do not appear to be important in ischemic preconditioning. Although a mast cell stabilizer such as DSCG can protect ischemic myocardium, it may do so by one of its other properties, e.g., membrane stabilization.

Animals↗
PubMed1998

Bioactivities and secondary structure of mast cell degranulating (MCD) peptide analogs.

Three analogs of Mast Cell Degranulating (MCD) peptide with C-terminal and one analog with N- and C-terminal deletions were synthesized and assayed for histamine-releasing activity in mast cells. Des(20-22)-MCD and des(21)-MCD markedly decreased this activity. In des(16-17,21)-MCD this activity was completely abolished. By contrast, when the C- and N-termini were truncated in des(1-2,20-22)-MCD, the full activity of MCD peptide was restored. The possibility that these analogs trigger or inhibit oxygen radicals from neutrophils was examined in a cell-free system with a chemiluminescence assay. None of the above analogs exhibited inflammatory or anti-inflammatory activity. Changes in biological activities were correlated with structural changes, as seen by circular dichroism (CD) spectroscopy.

Amino Acid Sequence↗
PubMed1984

Late phase bronchial obstruction following nonimmunologic mast cell degranulation.

Immunologic degranulation of airway mast cells after antigen inhalation produces early and late airway obstructions in allergic sheep. In this study we determined whether nonimmunologic degranulation of airway mast cells by inhalation of compound 48/80 had similar effects. In five sheep, pulmonary flow resistance (RL), thoracic gas volume (Vtg), and arterial O2 tension (Pao2) were determined prior to and at predetermined times after inhalation of 48/80 aerosol. Immediately after challenge mean specific lung resistance (sRL = RL X Vtg) increased by 259% and mean Pao2 decreased by 29%. All values returned to normal by 3 h. By 5-h postchallenge sRL again increased significantly; this second increase in sRL (92% above base line) was maximal at 7 h and was accompanied by a 17% drop in Pao2. In these same sheep inhalation of Ascaris suum antigen produced comparable early changes in sRL, but the onset of the late response was somewhat delayed and more pronounced. In a second group of sheep (n = 5), pretreatment with the mast cell stabilizer cromolyn sodium prevented both early and late responses by compound 48/80. Pretreatment with the histamine H1-antagonist chlorpheniramine had no significant effect on either response, whereas pretreatment with FPL 55712, an antagonist of slow-reacting substance of anaphylaxis (SRS-A), slightly but not significantly attenuated the early response and completely prevented the late response. We conclude that, like immunologic stimuli, nonimmunologic mast cell degranulation produces early and late bronchial obstructions in allergic sheep; that these responses are mediator dependent; and that while histamine and SRS-A contribute to the early response, it is the early appearance of SRS-A which is an important prerequisite for the late response.

Airway Obstruction↗
PubMed2001

Further studies on the structural requirements for mast cell degranulating (MCD) peptide-mediated histamine release.

Mast cell degranulating (MCD) peptide was modified in its two disulfide bridges and in the two arginine residues in order to measure the ability of these analogs to induce histamine release from mast cells in vitro. Analogs prepared were [Ala(3,15)]MCD, [Ala(5,19)]MCD, [Orn(16)]MCD, and [Orn(7,16)]MCD. Their histamine-releasing activity was determined spectrofluorometrically with peritoneal mast cells. The monocyclic analogs in which the cysteine residues were replaced pairwise with alanine residues showed three-to ten-fold diminished histamine-releasing activity respectively, compared with the parent MCD peptide. Substantial increases in activity were observed where arginine residues were replaced by ornithines. The ornithine-mono substituted analog showed an almost six-fold increase and the ornithine-doubly substituted analog three-fold increase in histamine-releasing activity compared with the parent MCD peptide. The structural changes associated with these activities were followed by circular dichroism (CD) spectroscopy. Changes in the shape and ellipticity of the CD spectra reflected a role for the disulfide bonds and the two arginine residues in the overall conformation and biological activity of the molecule.

Animals↗
PubMed1989

Acute intracerebroventricular injections of the mast cell degranulator compound 48/80 and behavior in rats.

The intracerebroventricular (ICV) injection of the mast cell degranulator Compound 48/80 (2.5-2.0 micrograms/kg) produced a marked behavioral syndrome in normotensive rats. The behaviors included head and body shakes, paw tremor, excessive grooming, unusual posture and gait, mild diarrhoea, piloerection, extreme agitation and irritability to touch, and a later phase of sedation. The highest doses (15 and 20 micrograms/kg) also produced catalepsy and episodes of "barrel rolling" (continuous rolling of 1-8 turns around the longitudinal axis). These behaviors were observed for approximately 15-30 min although the sedation and catalepsy were maintained for 90-120 min. A second ICV injection of the 10 micrograms/kg dose of Compound 48/80 given 2 hr after an initial injection of this dose, produced a much reduced response and the numbers of head and body shakes, and episodes of paw tremor and grooming were between 20-30% of those produced by the first injection. The reduced effect of the second injection indicates that the behavioral effects of Compound 48/80 may arise from the acute degranulation of mast cells rather than direct effects on neuronal populations or the cerebral vasculature.

Animals↗
PubMed1990

Mast cell degranulating peptide: a multi-functional neurotoxin.

This review discusses our present knowledge of the structure and activities of the mast cell degranulating peptide (MCDP). This peptide is a basic, 22 amino acid residue component of honey bee venom with striking immunological and pharmacological activities. MCDP is a potent anti-inflammatory agent, but at low concentrations it is a strong mediator of mast cell degranulation and histamine release. MCDP is also an epileptogenic neurotoxin, an avid blocker of the potassium channels and can cause a significant lowering of the blood pressure in rats. Some of the biological activities of MCDP appear to have distinct mechanisms and may represent a good illustration of the structure-function relationship.

Amino Acid Sequence↗
PubMed1997

Effect of administration of malathion for 14 days on macrophage function and mast cell degranulation.

Previous studies have shown that acute, oral administration of malathion modulated the humoral immune response to T-cell-dependent antigen, mitogenic responses, macrophage function, and mast cell degranulation. While administration of malathion for 14 days did not affect the generation of an immune response to antigen, it was possible that macrophage and mast cell functions were affected. In this report, the effect of malathion administration for 14 days upon these parameters were assessed. This treatment regimen increased the respiratory burst capacity to a maximal level at a dose of 1 mg/kg/day or greater. The effect of oral administration of malathion for 14 days on the degranulation of mast cells in various organs (heart, skin, and small intestine) and peritoneal lavage fluid was also assessed. At doses of 1 mg/kg/day and above, the number of mast cells that was undegranulated decreased and the number that was severely degranulated increased. There was no change in mast cell integrity in biopsies from heart and skin, and in peritoneal fluid after 14-day administration of 0.1 mg/kg/day. However, the number of mast cells associated with the small intestine that had undergone degranulation was increased at this dose of malathion. These data indicate that repeated administration of malathion increased macrophage function at doses as low as 1 mg/kg/day and led to mast cell degranulation at doses as low as 0.1 mg/kg/day.

Animals↗
PubMed2002

A comparison of reactive oxygen species generation by rat peritoneal macrophages and mast cells using the highly sensitive real-time chemiluminescent probe pholasin: inhibition of antigen-induced mast cell degranulation by macrophage-derived hydrogen peroxide.

Mast cells and macrophages live in close proximity in vivo and reciprocally regulate one another's function in various ways. Although activated macrophages possess a powerful reactive oxygen species (ROS) generating system, there is conflicting evidence regarding whether mast cells can produce ROS. We used the highly sensitive real-time chemiluminescent probe Pholasin to examine ROS release by peritoneal macrophages and mast cells isolated from OVA-sensitized rats. Macrophages stimulated with PMA (0.8 microM) or ionomycin (1 microM), but not OVA (1 microg/ml), released high-level ROS, levels of which peaked after 3-7 min and declined to baseline levels within 1 h. Superoxide was identified as the major ROS species induced by PMA but not by ionomycin. In contrast, purified mast cells stimulated with PMA released low-level ROS, which was entirely due to the contaminating (2%) macrophages, and did not release any detectable ROS in response to ionomycin or OVA at concentrations that induced degranulation. Stimulation of mixed cell populations with PMA to induce macrophage ROS release led to 50% inhibition of serotonin release from mast cells stimulated 5 min later with OVA. The PMA-induced inhibitory factor was identified as hydrogen peroxide. In conclusion, activated rat peritoneal macrophages but not mast cells produce ROS, and macrophage-derived hydrogen peroxide inhibits mast cell degranulation. The latter could be an important mechanism whereby phagocytic cells regulate mast cell activation and promote resolution of IgE-mediated inflammation.

Animals↗
PubMed1997

Elimination of a primary schistosome infection from rats coincides with elevated IgE titres and mast cell degranulation.

Schistosomes are eliminated from laboratory rats around 28 days post-infection, whilst they are still resident within the hepatic portal distributaries of the liver. We have previously shown that their presence in this location is accompanied by an intense mastocytosis. We have investigated the potential relationships between IgE responses, the allergenicity of schistosome antigens, mast cell responsiveness, and worm elimination. Total and specific IgE were measured using an ELISA and a functional assay based on 3H serotonin release from activated rat basophilic leukemia cells (RBL-SRA), respectively. Both assays revealed that infected rats produced elevated IgE titres relative to naive animals. At days 28 and 35, mixed-sex infections stimulated a higher total IgE than male-only infections. IgE was affinity purified from rat infection serum and used to probe a fractionated soluble worm antigen preparation (SWAP) by Western blotting. Two allergenic products were detected of M(r) 67 and 36-38 kDa, the former having the same molecular weight as a previously identified secretory protein. IgE from mixed-sex schistosome infections bound strongly to the 36-38 kDa molecule, compared to the relatively weak binding exhibited by IgE from male-only infection serum. Since eggs were not recovered from the infected rats, this reactivity was attributed to the greater release of allergens from female worms. Results from the RBL-SRA showed that female SWAP was a more effective trigger of mast cell degranulation in vitro, for equal amounts of protein. This enhanced allergenicity was ascribed to the relative abundance of carbohydrate moieties. Our results support a role for IgE, and mast cell degranulation in the elimination of a primary schistosome burden from rats.

Allergens↗
PubMed1997

Effect of administration of malathion for 90 days on macrophage function and mast cell degranulation.

Previous studies have shown that acute, oral administration of malathion modulated the humoral immune response to T cell-dependent antigen, mitogenic responses, macrophage function and mast cell degranulation. In this report, the effects of malathion administration for 90 days on macrophage function, as measured by respiratory burst capacity, phagocytic capability and the production of cathepsin D, and mast cell integrity were assessed. A dose-dependent increase in respiratory burst activity was observed at all doses tested. The production of cathepsin D was elevated at doses of 1 mg/kg/day malathion or greater. The phagocytic capability of peritoneal macrophages was elevated at the dose of 0.1 mg/kg/day, but was suppressed at higher doses. The effect of oral administration of malathion for 90 days on the degranulation of mast cells, in both organs (skin and uterus) and peritoneal lavage fluid, was also assessed. Degranulation (both severe and slight) of mast cells from the skin and peritoneum was observed at a dose of 1.0 mg/kg/day or greater. In addition, the percentage of mast cells that were undegranulated was decreased. In the skin, but not the peritoneum, these effects were dose-dependent. In the uterus, the percentage of mast cells that were undegranulated was decreased and severely degranulated was increased at a dose of 0.1 mg/kg/day or greater. These data indicate that repeated administration of malathion increased macrophage function and led to mast cell degranulation at doses as low as 0.1 mg/kg/day for 90 days.

Administration, Oral↗
PubMed1984

Induction of human cutaneous mast cell degranulation by opiates and endogenous opioid peptides: evidence for opiate and nonopiate receptor participation.

In order to examine the capacity of pharmacologically useful opiates to stimulate human mast cell secretion, subjects were skin tested with morphine, codeine, or meperidine hydrochloride. All three agents acted equipotently in eliciting positive immediate skin reactions from all subjects tested. Each agent demonstrated 10 mm of net whealing at 5 to 10 micrograms base (16.7 to 40.4 nmol) injected intradermally. The ability to elicit immediate skin test reactions with endogenous opioid peptides was examined with the use of dynorphin, [D-Ala, 2-D-Leu5] enkephalin, beta-endorphin, and morphiceptin . All four compounds induced wheal-and-flare reactions with the order of potency: dynorphin, greater than beta-endorphin, and greater than [D-Ala, 2-D-Leu5] enkephalin approximately equal to morphiceptin at dose ranges of 0.3 to 8.45 nmol. The inhibition of reactivity by hydroxyzine and the demonstration of mast cell degranulation by electron microscopy suggest that the immediate skin responses to opioid stimulation occur as a consequence of mast cell degranulation. Experiments with the opioid receptor antagonist, naloxone, suggest that both opioid and nonopioid receptors may be involved. These results imply that endogenous opioid peptides possibly may play a role in mast cell function and/or degradulation .

Codeine↗
PubMed2004

Tanshinones inhibit mast cell degranulation by interfering with IgE receptor-mediated tyrosine phosphorylation of PLCgamma2 and MAPK.

Recently we have isolated four active components from Tanshen (the root of Salvia miltiorrhiza Bunge, Labiatae) responsible for the anti-allergic activities. In this study, the molecular mechanism of action of tanshinones for the inhibition of mast cell degranulation was investigated by testing their effects on the signaling components of the high affinity IgE receptor FcepsilonRI. Activation of FcepsilonRI produced immediate tyrosine phosphorylation of Syk, mitogen-activated protein kinase extracellular signal-regulated kinase, ERK1/ERK2 (p44, p42), and phospholipase Cgamma2 (PLCgamma2). 5,16-Dihydrotanshinone-I possessed the strongest inhibitory effects on mast cell degranulation and markedly reduced FcepsilonRI-mediated tyrosine phosphorylation of ERK and PLCgamma2. This suggests that tanshinones possibly exert their anti-allergic activities by affecting FcepsilonRI-mediated tyrosine phosphorylation of ERK and PLCgamma2. Abbreviations. FcepsilonRI:high affinity IgE receptor ERK:extracellular signal regulated kinase PLC: phospholipase C

Animals↗