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PubMed1979

Ultrastructural observations on mast cell degranulation and its prevention.

The surface alterations of rat peritoneal mast cells during degranulation induced by calcium chloride (CaCl2) and its prevention by salbutamol sulfate (Sal. Sulf.), chlorpheniramine maleate (CM), and disodium cromoglycate (DSCG) were followed with a scanning electron microscope. CaCl2 caused a protuberation of the cytoplasmic granules already after 30 s, an advanced degranulation after 60-75 s, and a complete destruction of the cells after 180 s of incubation. The degranulation process was prevented by Sal. Sulf., CM, and DSCG. A comparison of the surface changes induced by these agents with the ultrastructural findings observed with a transmission electron microscope showed that neither Sal. Sulf. nor CM prevented the alterations of the internal structure of the cells, suggesting that these substances act mainly on the cytoplasmic membrane. The best prevention for both the surface and the internal structure of the cells was obtained by DSCG, indicating that this substance is a stabilizer of both membrane and internal organelles of the mast cells.

Albuterol↗
PubMed1980

Elevated blood histamine levels and mast cell degranulation in solar urticaria.

1 Ultraviolet radiation (UVR)-induced wealing was studied in four patients with solar urticaria, whose measured action spectra were within the range 300 to 700 nm. 2 Elevated histamine levels were found in blood draining wealed skin in all four patients. 3 Histological and electron microscopial studies of the irradiated skin showed evidence of mast cell degranulation. 4 These findings demonstrate an association between histamine release from mast cells and wealing in solar urticaria, and should encourage evaluation of drugs which suppress histamine release in this disorder.

Adult↗
PubMed2001

SHIP's C-terminus is essential for its hydrolysis of PIP3 and inhibition of mast cell degranulation.

The SH2-containing inositol-5'-phosphatase, SHIP, restrains bone marrow-derived mast cell (BMMC) degranulation, at least in part, by hydrolyzing phosphatidylinositol (PI)-3-kinase generated PI-3,4,5-P(3) (PIP3) to PI-3,4-P(2). To determine which domains within SHIP influence its ability to hydrolyze PIP3, bone marrow from SHIP(-/-) mice was retrovirally infected with various SHIP constructs. Introduction of wild-type SHIP into SHIP(-/-) BMMCs reverted the Steel factor (SF)-induced increases in PIP3, calcium entry, and degranulation to those observed in SHIP(+/+) BMMCs. A 5'-phosphatase dead SHIP, however, could not revert the SHIP(-/-) response, whereas a SHIP mutant in which the 2 NPXY motifs were converted to NPXFs (2NPXF) could partially revert the SHIP(-/-) response. SF stimulation of BMMCs expressing the 2NPXF, which could not bind Shc, led to the same level of mitogen-activated protein kinase (MAPK) phosphorylation as that seen in BMMCs expressing the other constructs. Surprisingly, C-terminally truncated forms of SHIP, lacking different amounts of the proline rich C-terminus, could not revert the SHIP(-/-) response at all. These results suggest that the C-terminus plays a critical role in enabling SHIP to hydrolyze PIP(3) and inhibit BMMC degranulation.

Amino Acid Motifs↗
PubMed2000

A BASH/SLP-76-related adaptor protein MIST/Clnk involved in IgE receptor-mediated mast cell degranulation.

Cross-linking of the high-affinity IgE receptor (FcepsilonRI) on mast cells by IgE-antigen complex triggers signal transduction cascades leading to the release of inflammatory mediators and production of cytokines, which are critical for the development of allergic reactions. We have identified a novel member of the BASH/SLP-76 immunoreceptor-coupled adaptor family expressed in mast cells, termed MIST (for mast cell immunoreceptor signal transducer), which has later been found to be identical to a recently reported cytokine-dependent hemopoietic cell linker, Clnk. Upon FcepsilonRI cross-linking, MIST/Clnk is tyrosine phosphorylated and associates with signaling proteins, phospholipase Cgamma, Vav, Grb2 and linker for activation of T cells (LAT). Overexpression of a mutant form of MIST/Clnk inhibited FcepsilonRI-mediated degranulation, increase in intracellular Ca(2+), NF-AT activation and phosphorylation of LAT. As a crucial signaling component for FcepsilonRI-induced mast cell degranulation, MIST/Clnk might serve as a target for anti-allergic therapy.

Adaptor Proteins, Signal Transducing↗
PubMed1985

Exercise-induced anaphylaxis: a serious form of physical allergy associated with mast cell degranulation.

Exercise-induced anaphylaxis (EIA) is a unique and an increasingly recognized syndrome consisting of premonitory symptoms and signs of generalized body warmth, pruritus, and erythema, which progresses on continued exertion to confluent urticaria, laryngeal edema with stridor or hoarseness, and gastrointestinal colic and frequently culminates in vascular collapse. Previous studies of five individuals with this condition have demonstrated significant elevations of serum histamine concurrent with the early clinical manifestations after experimental exercise. To assess relevant morphologic alterations in the skin of these patients, cutaneous mast cells were examined by light and transmission electron microscopy before and during the initial erythema elicited by exertion. The marked alterations observed in mast cells immediately after exercise consisted of (1) loss of electron density and internal substructure of granules, (2) fusion of granule membranes with those of adjacent granules and with mast cell membranes creating conduits to the extracellular space, and (3) an apparent decrease in the number of intact granules per cell. Biopsy specimens obtained before exercise from patients with EIA and from two normal individuals who served as control subjects were identical, and the control subjects had normal mast cell morphology after exercise. Serum histamine levels were significantly elevated in patients with EIA after exercise at the time of biopsy, whereas control subjects had normal levels. These observations provide evidence that EIA is a distinct form of physical allergy associated with mast cell degranulation similar in morphology to that of human pulmonary mast cell IgE-Fc-dependent activation secretion. Characterization of this disorder is important because its prevalence may be underestimated, and its clinical consequences, which may include some morbidity, are not fully known.

Adult↗
PubMed1985

Alterations in mast cell degranulation and ovarian histamine in the proestrous hamster.

Mast cells in the ovary of cyclic hamsters were observed exclusively in the hilum and in the vicinity of blood vessels that enter and exit the ovary. Ovaries were collected on proestrus from hamsters at 0900 h preluteinizing hormone (LH) surge, 1500 h (peak LH surge), and 2100 h (post-LH surge) and processed for routine histologic staining with toluidine blue. A significant increase in the percentage of extensively degranulating mast cells was observed coincident with the gonadotropin surge (0900 h: 5.39 +/- 0.97%; 1500 h: 20.39 +/- 2.76%). At the peak of the LH surge the ovarian histamine concentration was also significantly higher than those before and after the surge (1500 h: 5.13 +/- 0.94 ng/mg ovary; 0900 h and 2100 h: 2.84 +/- 0.35 and 3.02 +/- 0.48 ng/mg, respectively). The results indicate that a major source of ovarian histamine may be mast cells residing in the ovarian hilum and surrounding the ovarian blood vessels that enter and exit the ovary. In addition, the gonadotropin surge on the day of proestrus may be a trigger for release of mast cell histamine.

Animals↗
PubMed1991

Paneth cell degranulation and lysozyme secretion during acute equine alimentary laminitis.

The equine Paneth cell response to a shift in the microbial balance of the intestinal tract was studied by inducing an acute episode of alimentary laminitis in 6 mature ponies. The normal bacterial population of the gut was modified by administration of a carbohydrate-rich ration. During acute laminitis a dramatic degranulation of the Paneth cells occurred in the intestinal glands throughout the duodenum, jejunum, and ileum. Bacteriocidal lysozyme, which was immunohistochemically identified as a component of the Paneth cell secretory granule, was evident in the glandular lumina and in degranulated Paneth cells. These results indicate that lysozyme is secreted by the equine Paneth cell in an apparent attempt to regulate the changing microbial population induced by carbohydrate overload of the gut. From these observations, it is suggested that the Paneth cell plays a role in the mucosal defense system of the equine intestinal tract.

Animals↗
PubMed1995

Ultraviolet B irradiation of skin induces mast cell degranulation and release of tumour necrosis factor-alpha.

In the 'sunburn' response in skin, dermal blood vessels are activated and traffic of dendritic Langerhans' cells altered. While these changes have been attributed to the cytokine TNF-alpha, the source of this acutely released TNF has not been identified. This report demonstrates that the 'sunburn' response, both in vivo and in vitro, is accompanied by rapid degranulation of cutaneous mast cells, with consequential release of intracellular stores of TNF. Epidermal keratinocytes were only minor contributors to local TNF production. Expression of the TNF-inducible CD62E (E-selectin/ELAM-1) and CD54 adhesion molecules on cutaneous endothelium occurred 2 h following mast cell degranulation, and this event was sensitive to blockade of mast cells with disodium cromoglycate. These results indicate that TNF release in skin in the acute sunburn response can largely be attributed to mast cells.

Adult↗
PubMed1988

Inhibition of beta-bungarotoxin binding to brain membranes by mast cell degranulating peptide, toxin I, and ethylene glycol bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid.

The presynaptically active snake venom neurotoxin beta-bungarotoxin (beta-Butx) is known to affect neurotransmitter release by binding to a subtype of voltage-activated K+ channels. Here we show that mast cell degranulating (MCD) peptide from bee venom inhibits the binding of 125I-labeled beta-Butx to chick and rat brain membranes with apparent Ki values of 180 nM and 1100 nM, respectively. The mechanism of inhibition by MCD peptide is noncompetitive, as is inhibition of 125I-beta-Butx binding by the protease inhibitor homologue from mamba venom, toxin I. Beta-Butx and its binding antagonists thus bind to different sites of the same membrane protein. Removal of Ca2+ by ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid inhibits the binding of 125I-beta-Butx by lowering its affinity to brain membranes.

Animals↗
PubMed1985

Dynamics of mast cell degranulation in human allergic nasal epithelium after provocation with allergen.

The histamine content in the nasal epithelial layer of twenty-five patients with nasal allergy was measured before, 10 min after and 1 hr after nasal provocation with allergen. A decrease in histamine content was observed 10 min after provocation compared to the values obtained before provocation (P less than 0.05). There was a tendency for an increase in the histamine content of the nasal epithelium one hour after provocation when compared with the amounts present 10 min after provocation (P less than 0.1). Mast cells in the nasal epithelial layer of a further five patients were studied by electron microscopy 10 min and 1 hr after provocation. The rate of mast cell degranulation appeared to decrease 1 hr after provocation when compared with 10 min. Our study suggests that some mast cells commence their migration to the nasal epithelial layer over a short time period and that they may play a role in the onset of the allergic nasal reaction in patients with allergic nasal symptoms.

Adolescent↗
PubMed1987

Isolation and structure analysis of bee venom mast cell degranulating peptide.

The venom of Apis mellifera was processed by gel permeation chromatography on Sephadex G-50 and by reversed-phase HPLC. The initial gel permeation step was carried out in the presence of phosphate ions (0.5 M). Ion pair reagents were required to resolve the strongly basic peptides, secapin, mast cell degranulating (MCD-) peptide and apamin, by reversed-phase (RP) HPLC. Using this relatively simple procedure it is possible to isolate these peptides essentially free of melittin (less than 1 in 10(7)) and phospholipase (less than 1 in 10(5] in high yield. The CD spectrum and secondary structure analysis are reported for MCD-peptide and on this basis a solution structure is proposed for this toxin.

Animals↗
PubMed1991

Riluzole prevents hyperexcitability produced by the mast cell degranulating peptide and dendrotoxin I in the rat.

Using electroencephalographic (EEG) recordings in freely moving rats and extracellular neuronal firing-rate recordings in hippocampal slices, we examined the effects of riluzole (RP 54274), a compound with anti-glutamate properties, against the convulsive seizures and the cellular hyperexcitability produced by the mast-cell degranulating peptide (MCD), dendrotoxin I (DTXi) and 4-aminopyridine (4-AP). I.c.v. administration of riluzole (10 nmol) prevented the seizures induced by MCD, and to a lesser extent those due to DIXi, whilst leaving 4-AP seizures unaffected. This effect was also present after oral administration of the compound (4 mg kg-1) and lasted for approximately 6 h. Electrophysiological recordings in vitro confirmed that riluzole dose dependently and reversibly abolished the sustained increase in firing rate induced by both MCD and DTXi in the hippocampus. These results indicate that the anti-epileptic spectrum of riluzole in this model has similarities with, but is not identical to, that of classical potassium channel openers, and differs from that of calcium channel blockers or other glutamate antagonists such as D(-)-2-amino-5-phosphono-valeric acid. However, since MCD releases glutamate, the preventive effect of riluzole in this model may involve direct or indirect interaction with glutamatergic processes.

4-Aminopyridine↗
PubMed1982

Do mast cell degranulators release prostaglandins from frog atria?

Isolated atria of frogs responded to compound 48/80 and d-tubocurarine with a delayed stimulation that showed tachyphylaxis and cross-tachyphylaxis indicating a common indirect mechanism. The blockers of H2-histamine, serotonin and beta-adrenergic receptors did not significantly antagonise these responses. However, in experiments with ex vivo and in vitro indomethacin-treated atria, the stimulant effects of mast cell degranulators were not observed, indicating a possible involvement of the prostaglandins.

Animals↗
PubMed1981

Mast cell degranulation in beige mice with the Chédiak-Higashi defect.

The degranulation response of peritoneal mast cells to calcium ionophore A23187 and compound 48/80 has been compared by scanning electron microscopy and transmission electron microscopy in normal C57 black mice and C57 beige mice with a genetic defect analogous to the human Chédiak-Higashi Syndrome (CHS). These methods reveal granule secretion in response to the degranulating agents in mast cells of both normal and beige mice. The observations indicate that beige peritoneal mast cells retain the capacity to exocytose their granules upon stimulation and suggest that the defect underlying the formation of the mega-inclusions is not attributable to impaired degranulation.

Animals↗
PubMed2004

NTAL phosphorylation is a pivotal link between the signaling cascades leading to human mast cell degranulation following Kit activation and Fc epsilon RI aggregation.

Aggregation of high-affinity receptors for immunoglobulin E (Fc epsilon RI) on the surface of mast cells results in degranulation, a response that is potentiated by binding of stem cell factor (SCF) to its receptor Kit. We observed that one of the major initial signaling events associated with Fc epsilon RI-mediated activation of human mast cells (HuMCs) is the rapid tyrosine phosphorylation of a protein of 25 to 30 kDa. The phosphorylation of this protein was also observed in response to SCF. This protein was identified as non-T-cell activation linker (NTAL), an adaptor molecule similar to linker for activated T cells (LAT). Unlike the Fc epsilon RI response, SCF induced NTAL phosphorylation in the absence of detectable LAT phosphorylation. When SCF and antigen were added concurrently, there was a marked synergistic effect on NTAL phosphorylation, however, SCF did not enhance the phosphorylation of LAT induced by Fc epsilon RI aggregation. Fc epsilon RI- and SCF-mediated NTAL phosphorylation appear to be differentially regulated by Src kinases and/or Kit kinase, respectively. Diminution of NTAL expression by silencing RNA oligonucleotides in HuMCs resulted in a reduction of both Kit- and Fc epsilon RI-mediated degranulation. NTAL, thus, appears to be an important link between the signaling pathways that are initiated by these receptors, culminating in mast cell degranulation.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Inhibition of mast cell degranulation by tanshinones from the roots of Salvia miltiorrhiza.

The activity-guided fractionation of the extract of the root of Salvia miltiorrhiza B. (Labiatae, Tanshen), led to the isolation of four active components responsible for the anti-allergic activity in vitro. Among them, 15,16-dihydrotanshinone-I and cryptotanshinone demonstrated significant inhibition of the release of beta-hexosaminidase from cultured RBL-2H3 cells in a dose-dependent manner; the IC50 values were calculated as 16 and 36 microM, respectively.

Animals↗
PubMed1980

Antigen-specific mast cell degranulation in contact sensitivity to picryl chloride. An early event.

Mast cells from the peritoneum of mice painted with the contact sensitizing agent picryl chloride degranulate when exposed to antigen (TNP) in vitro. Degranulation was consistently demonstrated 4 days after painting which associated with the ability of mice to produce contact sensitivity reactions as measured by ear swelling and radiometric assays. Serum reagin or reagin-producing cells could not be detected until 6 days after painting but TNP-phage neutralizing activity was detected after 2 days. Mast cell degranulation could be elicited by TNP or DNP derivatives indicating the involvement of antibody.

Animals↗