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PubMed1991

Mast cell degranulation and elastolysis in the early stage of striae distensae.

The lesions of nine patients with early striae distensae (SD) during puberty were examined by light and electron microscopy. Specific changes were seen in very early stage SD, and in clinically uninvolved skin 0.5 to 3 cm remote from the edge of the long axis of the SD lesions. Sequential changes of elastolysis accompanied by mast cell degranulation appeared first, followed by an influx of activated macrophages that enveloped fragmented elastic fibers. The relationships among elastic fibers, mast cells, and macrophages seen in the present work suggest their critical roles in the process of SD formation, especially in the early stage. Our results also indicate that the elastic fiber is the primary target of the pathological process, and the abnormalities extend as far as 3 cm beyond the lesion into normal skin.

Adolescent↗
PubMed2002

Protective effect of omeprazole against acute gastric mucosal lesions induced by compound 48/80, a mast cell degranulator, in rats.

Omeprazole, a proton pump inhibitor is known to function not only as a proton pump inhibitor but also as an anti-inflammatory agent, an antioxidant or a stimulator of gastric mucus secretion. We have shown that the pathogenesis of acute gastric mucosal lesions induced by compound 48/80, a mast cell degranulator, in rats involves neutrophil infiltration, lipid peroxidation, and mucin depletion, but not acid secretion, in the gastric mucosal tissue. Therefore, we examined whether omeprazole protects against acute gastric mucosal lesions induced by compound 48/80 in rats. Rats were injected with omeprazole (10 or 50 mgkg(-1), i.p.) at 0.5h before injection of compound 48/80 (0.75 mgkg(-1), i.p.). Omeprazole prevented gastric mucosal lesion development at 0.5 and 3h after compound 48/80 injection. Omeprazole attenuated decreased nonprotein sulfhydryl content and increased myeloperoxidase and xanthine oxidase (XO) activities and lipid peroxide (LPO) content in the gastric mucosa at 0.5h after compound 48/80 injection and increased myeloperoxidase and XO activities and LPO content, but not decreased hexosamine and adherent mucus contents, in the gastric mucosa at 3h. These results indicate that omeprazole protects against compound 48/80-induced acute gastric mucosal lesions in rats possibly through its anti-inflammatory and antioxidant actions.

Animals↗
PubMed1999

Mast cell degranulating (MCD) peptide: a prototypic peptide in allergy and inflammation.

The solid phase synthesis of mast degranulating peptide (MCD peptide) raised the possibility of preparing analogs and examining the pharmacology and the proposed role of this peptide as a potential agent in allergy and inflammation. MCD peptide, a cationic 22-amino acid residue peptide with two disulfide bridges, causes mast cell degranulation and histamine release at low concentrations and has anti-inflammatory activity at higher concentrations. Because of these unique immunologic properties, MCD peptide may serve as a useful tool for studying secretory mechanisms of inflammatory cells such as mast cells, basophils, and leukocytes, leading to the design of compounds with therapeutic potential.

Animals↗
PubMed1988

Mast cell degranulation and its inhibition by an anti-allergic agent tranilast. An electron microscopic study.

Degranulation of IgE-sensitized rat mast cells by antigen was studied quantitatively in vitro and in vivo by electron microscopy. The inhibition of this degranulation by an anti-allergic drug, N-(3,4-dimethoxycinnamoyl)anthranilic acid (Tranilast), was also examined both in vitro and in vivo. In the in vitro study using peritoneal mast cells, alteration of the granules, cavity formation by fusion of the perigranular membrane and granule discharge due to fusion of the cavity membrane with the cell membrane were observed and were accompanied by histamine release. Scanning electron microscopy disclosed the extrusion of smooth, round bodies from pores formed on the cell surface. In the in vivo study of passive cutaneous anaphylaxis (PCA), the characteristic features of mast cell degranulation were obvious 5 min after the injection of antigen; leakage of dye increased progressively from 5 to 30 min but was not found at 6 h. From quantitative analysis of the substructure of mast cells, it was demonstrated that degranulation of IgE-sensitized mast cell induced by antigen was achieved by sequential exocytosis both in vitro and in vivo. Tranilast inhibited these changes to a remarkable extent and it was concluded that the inhibition of mast cell degranulation by this drug might play an important role in anti-allergic treatment.

Animals↗
PubMed1994

Heparin prevents antigen-induced airway hyperresponsiveness: interference with IP3-mediated mast cell degranulation?

We hypothesized that heparin, because of its antiallergic and/or anti-inflammatory properties, modifies airway hyperresponsiveness (AHR). We studied the effects of inhaled heparin on AHR induced by specific antigen or by platelet-activating factor (PAF), a proinflammatory mediator. Specific lung resistance (sRL) was measured in 17 allergic sheep before, immediately after, and serially for up to 2 h after airway challenge with either specific antigen or PAF. Airway responsiveness was expressed as the cumulative provocative dose of carbachol that increased sRL to 4 cmH2O/s [PD4, in breath units (BU; 1 BU = 1 breath of 1% carbachol solution)]. PD4 was determined on a baseline day and on various experimental days 2 h after airway challenge with antigen or PAF, without or after pretreatment with inhaled heparin (1,000 U/kg). Pretreatment with inhaled heparin prevented antigen-induced bronchoconstriction and postantigen AHR. PD4 was 26 +/- 2.6 (SE), 12 +/- 1.7, and 22 +/- 2.8 BU on baseline, antigen control, and postheparin days, respectively. Heparin given immediately after the antigen challenge failed to modify the magnitude and/or duration of antigen-induced bronchoconstrictor response or postantigen AHR. Heparin also failed to prevent PAF-induced changes in sRL and AHR. In vitro heparin inhibited anti-immunoglobin E- and 1,4,5-inositol triphosphate-mediated degranulation of rat peritoneal mast cells without attenuating the effects of the Ca2+ ionophore A-23187. These data suggest that in "acute responders" heparin prevents antigen-induced bronchoconstriction and AHR, possibly by inhibiting 1,4,5-inositol triphosphate-dependent mast cell mediator release and not by its anti-inflammatory action.

Animals↗
PubMed1991

Mast Cell Degranulating Peptide Increases the Frequency of Spontaneous Miniature Postsynaptic Currents in CA3 Rat Hippocampal Neurons.

Mast cell degranulating peptide (MCDP) is a neurotoxic agent isolated from bee venom. It produces a long-term potentiation in the hippocampus. We now report that MCDP, at nanomolar concentrations, induces a reduction of a transient voltage-dependent potassium current (ID) in CA3 rat pyramidal neurons and a persistent (>30 min) enhancement of the frequency of spontaneous miniature excitatory and inhibitory postsynaptic currents (m.e.p.s.c.s. and m.i.p.s.c.s.). M.e.p.s.c.s. and m.i.p.s.c.s. were recorded in the presence of bicuculline (30 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), respectively. The increased frequency of m.e.p.s.c.s. (408 +/- 60%) and m.i.p.s.c.s. (583 +/- 553%) was independent of the reduction of ID because 4-aminopyridine (4-AP, 30 microM - 2 mM) blocked ID but had no effects on m.e.p.s.c.s. and m.i.p.s.c.s. In the presence of the calcium channel blocker manganese (3 mM), MCDP still enhanced the frequency of m.e.p.s.c.s. (326 +/- 162%). It is concluded that MCDP augments the release of excitatory and inhibitory transmitter by an action, which is independent of calcium influx, through voltage-dependent channels.

Journal Article↗
PubMed1984

Local histamine release after immunological and non-immunological mast cell degranulation in vivo.

Plasma histamine concentration in the circulation has been proposed as an index of mast cell degranulation occurring in vivo but there are problems with this approach in practice. Local elevations in plasma histamine occur in blood draining the site of antigen challenge in forearm skin. We have compared changes in plasma histamine concentration with time following intradermal injection of antigen, codeine or histamine to produce matched wheal and flare responses in 4 atopic subjects. Less histamine appears to be released after non-immunological challenge.

Adult↗
PubMed1980

[Basic peptides from bee venom, IV. Synthesis of the mast cell-degranulating peptide by liquid-phase fragment condensation (author's transl)].

The synthesis of the mast cell-degranulating peptide by liquid-phase fragment condensation is described. After the carboxyterminal of the peptide is condensated with polyethylene-glycol (Mr 10000) the following fragments are coupled stepwise on the polymer, a soluble carrier in dichloromethane by the dicyclohexylcarbodiimide/hydroxybenzotriazole-method. Pos. 17-21 Boc-Lys(Z)-Ile-Cys(SiPr)-Gly-Lys(Z) (I) Pos. 12-16 Boc-Pro-His(Trt)-Ile-Cys(Trt)-Arg(Tos) (II) Pos. 8-11 Boc-His(Trt)-Val-Ile-Lys(Z) (III) Pos. 5-7 Boc-Cys(SiPr)-Lys(Z)-Arg(Tos) (IV) Pos. 1-4 Boc-Ile-Lys(Z)-Cys(Trt)-Asn(Mbh) (V) It is practical to crystallize the polyethyleneglycol peptide-coupling products from ethanol after each step. Most of the protecting groups can be removed by treatment of the complete polyethylene-glycol-peptide in trifluoroacetic acid/HBr. In methanol, saturated with ammonia, the peptide is removed in the amid-form from the carrier. The guanidyl-blocking group disappears by solving the peptide in liquid HF. The crude peptide is converted into the tetra-S-sulfonate derivate by oxidative sulfitolysis and purified by ion-exchange and gel chromatography. After reduction by mercaptoethanol a cautious air-reoxidation of the SH- to the SS-peptide followed. Rechromatography on ion-exchange and dextran gels yields a peptide with good biological activity in rat cell histamin-liberation and inflammation inhibition compared with the natural recombinated product.

Amino Acid Sequence↗
PubMed1982

Gastric blood flow, mast cell degranulation and micromorphology of gastric mucosa following experimental haemorrhagic shock in dogs.

Ischaemia of the gastric mucosa in haemorrhagic shock appears to be one of the principal factors underlying acute bleeding from the upper gastrointestinal tract. In the present experimental study on dogs the changes of blood flow in the upper gastrointestinal tract were recorded by direct flow measurement in the pertinent vessels. Fourteen mongrel dogs were subjected to haemorrhagic shock lasting for 3 and 4 h. A decline of 46 per cent cardiac output was observed while coeliac artery blood flow decreased by 40 per cent and gastric artery blood flow by 60 per cent. All stages of stress ulcers were documented by light and electron microscopy. In addition, pronounced degranulation of mast cells preceding major tissue damage was observed. In the light of these findings a cascade of events is thought to be present resulting in the development of stress ulcer.

Animals↗
PubMed1989

Inhibition of in vitro and in vivo mast cell degranulation by Taenia crassiceps metacestodes in vitro incubation products.

In vitro released products of T. crassiceps metacestodes (TcIP) harvested from the peritoneal cavity of NMRI mice were tested for inhibitory effects on the in vitro degranulation of peritoneal mast cells (MCs) of normal mice (NMRI) and rats (Wistar) and on the in vivo degranulation of rat (Wistar) skin MCs (PCA-assay). In vitro degranulation was elicited chemically (compound 48/80, polymyxin B or the bee venom peptide, mellitin). In vivo degranulation was triggered immunologically (anaphylactic systems ovalbumin/anti-ovalbumin or Fasciola hepatica crude fluke extract antigen/serum of fluke-infected rats (Wistar]. In vitro degranulation of murine peritoneal MCs or the in vitro histamine release of rat peritoneal MCs normally induced chemically was significantly inhibited when the MCs were preincubated with the TcIP or with serum of T. crassiceps-infected NMRI mice from day 35 post infection and thereafter. In vitro degranulation of peritoneal MCs of infected mice was strongly inhibited beginning on day 10 after infection. Also in vivo degranulation of the IgE-sensitized rat skin MCs was significantly reduced by intradermal injection of the TcIP before (6, 3 and 1 h) antigen challenge and by preinjection (1 h) of serum from infected mice (day 80 p.i.)-The inhibitory effect was also demonstrated after immunoadsorption of mouse serum proteins naturally contaminating the TcIP. Heating (100 degrees C/15 min), even in the presence of 0.25 M HCl, did not suppress the inhibitory activity.

Animals↗
PubMed2000

Changes in histamine content following pharmacologically-induced mast cell degranulation in the rat conjunctiva.

Compound 48/80 was applied into one eye of male Wistar rats and a drop of vehicle into the contralateral eye. Another group of rats received sodium cromoglycate in both eyes every 6 h for a period of 48 h. One eye was challenged with compound 48/80 30 min after the end of treatment with sodium cromoglycate. The eyes were monitored clinically and the histamine content of the conjunctiva was determined fluorometrically. The basal histamine levels in rat conjunctival homogenates were quantified. Pharmacologically-induced mast cell degranulation by a single application of 0.1 g ml(-1)of compound 48/80 resulted in significant decreases of conjunctival histamine levels 1, 12 and 24 h after challenge. Sodium cromoglycate prevented the effect of compound 48/80 when administered into the eye prior to the challenge with the non-immunogenic histamine releaser. Upon termination of the application, the membrane stabilizer was unable to reverse the reduced histamine levels in the conjunctival homogenates.

Animals↗
PubMed1994

Effect of nonapeptide fragments of uteroglobin and lipocortin I on oedema and mast cell degranulation.

The anti-inflammatory action of nonapeptide fragments of uteroglobin or lipocortin I known as antiflammins, was tested in the carrageenan or phospholipase A2 rat paw oedema model. The development of carrageenan-induced oedema in rats was significantly inhibited during the early and late phases of the oedema by the local administration of antiflammins 1 and 2. However, the peptides were not able to inhibit phospholipase A2-induced oedema. The time course of the anti-oedematous activity of nonapeptides after intradermal carrageenan injection may be attributed to their effect on mast cell degranulation and accumulation and activation of leukocytes. Naja naja phospholipase A2 exhibited strong histamine release-inducing activity, which may have contributed to the rat paw oedema induction. Surprisingly, antiflammins had a limited but significant inhibitory effect on histamine secretion.

Animals↗
PubMed1992

Comparative effects of mast cell degranulators on perfused systemic blood vessels of Bufo melanostictus and Rana tigrina.

Three agents known to induce release of mast cell constituents, viz. polymyxin, compound 48/80 and polysorbate-80, were evaluated for effect on perfused blood vessels of R. tigrina and B. melanostictus. The mast cell degranulators caused vasoconstriction in frog and toad, except that for P-80 whose responses in toad were equivocal. Toads showed a general low responsiveness in comparison to frogs. Pharmacologic intervention with pheniramine, metergoline, hydergine, atropine and mecamylamine, respectively ruled out role of histamine, 5-HT, catecholamine or acetylcholine or even autonomic mechanisms in the above phenomena. The observations are suggestive of phylogenetic differences in biochemical profile of mast cells in amphibian species.

Animals↗
PubMed1986

[Effect of tomicide and the cell wall biopolymers of Streptococcus sp. Thom-1606 on mast cell degranulation].

The influence of tomicide and biopolymers obtained from the cell wall of Streptococcus sp. TOM-1606 on the degranulation of mast cells was studied. Among the biopolymers of the streptococcal cell-wall polysaccharide was shown to induce the highest destruction of mast cells (14.84 +/- 6.8%). The alteration of mast cells under the effect of peptidoglycan and teichoic acid was mildly positive (11.85 +/- 5.8% and 12.1 +/- 6.2%). At the same time the destruction induced by the complex of noninfectious allergen and the patient's serum was 33.2 +/- 3.8% respectively. Other preparations induced destruction on the level of spontaneous degranulation. The study of the action of the allergen-antibody complex in combination with tomicide and biopolymers obtained from the cell wall of Streptococcus sp. TOM-1606 revealed a decrease in the rate of mast cell degranulation almost to the background level (24.7 +/- 0.55% for the allergen-antibody complex and 8.4 +/- 4.2% to 11.8 +/- 5.3% for streptococcal biopolymers).

Animals↗
PubMed1986

Use of macrophage inhibition factor and mast-cell degranulation tests for diagnosis of cloxacillin-induced cholestasis.

Cloxacillin-induced cholestasis was diagnosed with the help of the macrophage inhibition factor and mast-cell degranulation tests. The simultaneous occurrence of both immediate type as well as cell-mediated hypersensitivity to the drug suggested that a defect in the histamine-induced suppressor cells may underly this cloxacillin-induced allergic reaction.

Cell Migration Inhibition↗
PubMed2004

Partial alanine scan of mast cell degranulating peptide (MCD): importance of the histidine- and arginine residues.

The influence of the two histidine and two arginine residues of mast cell degranulating peptide (MCD) in activity and binding was studied by replacing these amino acids in the MCD sequence with L-alanine. Their histamine releasing activity was determined on rat peritoneal mast cells. Their binding affinity to the FcepsilonRIalpha binding subunit of the human mast cell receptor protein, was carried out using fluorescence polarization. The histamine assay showed that replacement of His13 by Ala o ccurred without loss of activity compared with the activity of MCD. Alanine substitutions for Arg7 and His8 resulted in an approximately 40 fold increase, and for Arg16 in a 14-fold increase in histamine-releasing activity of MCD. The binding affinities of the analogs were tested by competitive displacement of bound fluorescent MCD peptide from the FcepsilonRIalpha binding protein of the mast cell receptor by the Ala analogs using fluorescence polarization. The analogs Ala8 (for His) and Ala16 (for Arg) showed the same binding affinities as MCD, whereas analog Ala7 (for Arg) and analog Ala13 (for His) showed slightly better binding affinity than the parent compound. This study showed that the introduction of alanine residues in these positions resulted in MCD agonists of diverse potency. These findings will be useful in further MCD structure-activity studies.

Alanine↗
PubMed1990

Mast cell degranulating peptide induces the expression of the c-fos proto-oncogene in hippocampus.

The intrahippocampal injection of the mast cell degranulating (MCD) peptide, a bee venom component acting on the K+ channel, results in the appearance of the proto-oncogene c-fos mRNA in the ipsi- and contralateral hippocampus of the treated animals without generating convulsions. This MCD-induced transcriptional event is discussed in terms of cellular plasticity since MCD peptide is known to induce long-term potentiation.

Animals↗