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PubMed1998

A blockade of complement activation prevents rapid intestinal ischaemia-reperfusion injury by modulating mucosal mast cell degranulation in rats.

We attempted to define the putative role of complement activation in association with mucosal mast cell (MMC) degranulation in the pathogenesis of rapid intestinal ischaemia-reperfusion (I/R) injury. We prepared complement activity-depleted rats by the administration of the anti-complement agent K-76COOH and the serine-protease inhibitor FUT-175. Autoperfused segments of the jejunum were exposed to 60 min of ischaemia, followed by reperfusion for various time periods, and the epithelial permeability was assessed by the 51Cr-EDTA clearance rate. The number of MMC was immunohistochemically assessed. In control rats, the maximal increase in mucosal permeability was achieved by 30-45 min of reperfusion. This increase was significantly attenuated by the administration of either K-76COONa alone or in combination with FUT-175. In contrast, the administration of carboxypeptidase inhibitor (CPI), which prevents the inactivation of complement-derived anaphylatoxins such as C5a, significantly enhanced the increase in I/R-induced mucosal permeability. These findings were confirmed morphologically by light microscopy and scanning electron microscopy. In addition, the I/R-induced mucosal injury was accompanied by a marked decrease in the number of MMC, and administration of K-76COOH significantly inhibited this change. These results indicate that complement activation and the generation of complement-derived anaphylatoxins are key events in I/R-induced mucosal injury. It is likely that intestinal I/R-induced mucosal injury may be partially mediated by MMC activation associated with the complement activation.

Anaphylatoxins↗
PubMed1983

New method for determination of mast cells degranulation in vitro. Effect of preimplantation embryos on mast cells.

A new method has been developed for determination of the degranulating activity of substances present in small volumes and exhibiting a low degranulating potency. By the use of this method MC degranulation was tested, induced by preimplantation of mouse embryos. It was found that old morulae and young blastocysts (4th day of pregnancy) contain a factor which reacts with MC causing extrusion of cytoplasmic grains. It is suggested that degranulation activity may be connected with the formation of a new, biologically active compounds thus with the biochemical differentiation of the embryos.

Animals↗
PubMed1984

Mast cell degranulation in the evolution of acute eruptive guttate psoriasis vulgaris.

Clinically normal psoriatic skin (CNPS) and psoriatic lesions (PLs) were studied for mast cell degranulation (MCD) in patients with acute eruptive guttate psoriasis vulgaris (AEGP) following penicillin-treated acute streptococcal throat infection. The clinically manifest duration of psoriasis at the time of the biopsies was 2, 5, 10, 14, or 21 days. Two types of MCD were distinguished. Type I was characteristic for those portions of the CNPS in which vascular and epidermal changes were detected, while the PLs showed both Type I and Type II MCD. In Type I MCD the extruded granules (MCGs) in the immediate vicinity of the mast cells appeared as intact bodies encased in a distinctly trilaminar membrane. Around subepidermal and subpapillary blood vessels, in stratum papillare without proximity of blood vessels, beneath the epidermal-dermal junction, in lamina lucida, and in intercellular space of strata basale and spinosum the MCGs appeared partly as intact structures and partly in more or less disintegrated form. In Type II MCD the MCGs were extruded without perigranular membranes. The data here presented showed that MCD is an early and constant feature in the evolution of AEGP.

Acute Disease↗
PubMed1992

Mechanism of the modulation of murine peritoneal cell function and mast cell degranulation by low doses of malathion.

Malathion is a widely used organophosphate pesticide that modulates immune function at noncholinergic doses. Previous studies showed that this alteration in immune function was the result of enhanced macrophage function. In the present study, the effects of low doses of purified malathion (as low as 0.25 mg/kg malathion) administered orally to mice enhanced the respiratory burst of peritoneal cells. Microscopic examination of the peritoneal cells showed that mast cells were degranulated within 4 hr after malathion administration. The amount of beta-hexosaminidase, an enzyme released upon immunologic degranulation of mast cells, in the peritoneal lavage fluid of malathion-treated mice was also significantly elevated with 4 hours after malathion administration. Treatment of RBL-1, a rat basophilic cell line, cells with malathion, parathion or paroxon in vitro also led to the release of beta-hexosaminidase with paraoxon being the most potent. Further examination of the peritoneal cells of malathion-treated mice showed that the percentage of phagocytic peritoneal cells ingesting mast cell granules and the number of granules ingested per cell were elevated. These data suggest that malathion may enhance the respiratory burst of peritoneal cells through degranulation of peritoneal mast cells and the subsequent exposure to peritoneal cells to mast cell mediators.

Animals↗
PubMed1990

Dermal mast cell degranulation in systemic sclerosis.

Paired biopsy samples from involved and uninvolved skin were obtained from 19 patients with generalized scleroderma (11 with early, progressive disease and 8 with late, improving disease). Skin biopsy samples were double stained for mast cell granules and for mast cell membrane. The number of mast cells was increased in patients with systemic sclerosis (SSc), in both involved and uninvolved skin and in both early and late disease. There was an increase in the number of degranulated mast cells in the involved skin of patients with both early and late disease and in the not-yet-involved skin of patients with early disease; however, there was no increase in the number of degranulated mast cells in areas of previously involved but now normal skin of patients with late disease. Increases in mast cell number and degranulation precede clinically apparent dermal fibrosis in SSc. These observations and the absence of mast cell degranulation in regressing skin suggest a participatory role of the mast cell in the clinical progression of skin changes in SSc.

Adult↗
PubMed2005

Mitochondrial Ca2+ flux is a critical determinant of the Ca2+ dependence of mast cell degranulation.

An increase in intracellular Ca2+ ([Ca2+]i) is necessary for mast cell exocytosis, but there is controversy over the requirement for Ca2+ in the extracellular medium. Here, we demonstrate that mitochondrial function is a critical determinant of Ca2+ dependence. In the presence of extracellular Ca2+, mitochondrial metabolic inhibitors, including rotenone, antimycin A, and the protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), significantly reduced degranulation induced by immunoglobulin E (IgE) antigen or by thapsigargin, as measured by beta-hexosaminidase release. In the absence of extracellular Ca2+; however, antimycin A and FCCP, but not rotenone, enhanced, rather than reduced, degranulation to a maximum of 76% of that observed in the presence of extracellular Ca2+. This enhancement of extracellular, Ca2+-independent degranulation was concomitant with a rapid collapse of the mitochondrial transmembrane potential. Mitochondrial depolarization did not enhance degranulation induced by thapsigargin, irrespective of the presence or absence of extracellular Ca2+. IgE antigen was more effective than thapsigargin as an inducer of [Ca2+]i release, and mitochondrial depolarization augmented IgE-mediated but not thapsigargin-induced Ca2+ store release and mitochondrial Ca2+ ([Ca2+]m) release. Finally, atractyloside and bongkrekic acid [an agonist and an antagonist, respectively, of the mitochondrial permeability transition pore (mPTP)], respectively, augmented and reduced IgE-mediated Ca2+ store release, [Ca2+]m release, and/or degranulation, whereas they had no effects on thapsigargin-induced Ca2+ store release. These data suggest that the mPTP is involved in the regulation of Ca2+ signaling, thereby affecting the mode of mast cell degranulation. This finding may shed light on a new role for mitochondria in the regulation of mast cell activation.

Animals↗
PubMed1984

Ultrastructure of mast cell degranulation induced by eosinophil peroxidase: Use of diaminobenzidine cytochemistry by scanning electron microscopy.

It has been previously demonstrated that eosinophil peroxidase (EPO) when supplemented with hydrogen peroxide and a halide induces noncytotoxic mast cell degranulation. Using a more highly purified EPO preparation, the ultrastructure of EPO-induced mast cell secretion has been studied using transmission and scanning electron microscopy and freeze-fracture techniques. At relatively low EPO concentrations, secretory changes were comparable to those caused by other mast cell secretagogues. Swollen and less electron-dense granules were seen in intracellular channels, some of which opened to the outside of the cell. EPO stimulation led to bulging of the surface membrane by submembranous granules and formation of pores in the cell surface that also contained fewer villous projections than control cells. During the secretory process, plasma membrane bulges were depleted of intramembranous particles in both the E and P faces of the apical regions of the perigranular and plasma membranes. Higher EPO concentrations caused a marked cytotoxic disruption of the mast cells. Diaminobenzidine cytochemistry was used to detect EPO reaction products on the mast cell surface by scanning electron microscopy; this technique should prove useful in detecting peroxidase reaction products on a variety of target cells.

Animals↗
PubMed1980

T cell-dependent mast cell degranulation and release of serotonin in murine delayed-type hypersensitivity.

We have previously suggested that the release of serotonin (5-hydroxytryptamine) (5-HT) by local tissue mast cells is required for the elicitation of delayed-type hypersensitivity (DTH) in mice. In the current study, light microscopic radioautographs from animals treated with [3H]5-HT indicated that local mast cells released 5-HT between 6 and 18 h during the evolution of DTH. Ultrastructural examination of mast cells revealed surface activation, indicated by extension of surface filopodia, and degranulation by fusion and exocytosis. Light and electron microscopic studies of the endothelium of postcapillary venules at sites of DTH revealed the development of gaps between adjacent cells. The development of gaps permitted extravasation of tracers that was abolished by depletion or antagonism of 5-HT. Thus mast cells degranulated and released 5-HT in DTH, and this 5-HT acted on local vessels. Recipients of nonadherent, non-immunoglobulin-bearing sensitized lymphocytes also demonstrated similar mast cell degranulation and the formation of endothelial gaps. This indicated that mast cell degranulation and 5-HT release in murine DTH were probably T cell dependent.

Animals↗
PubMed2003

In vitro inhibition of human conjunctival mast-cell degranulation by ketotifen.

Ketotifen relieves the symptoms of allergic conjunctivitis through multiple mechanisms of action. One such mechanism may involve stabilization of conjunctival mast cells. Because of inter- and intra-species variation, however, this hypothesis cannot be adequately tested using mast cells from animals or other human tissues. We therefore employed human conjunctival mast cells. The mast cells were prepared using human conjunctival tissues obtained from US eye banks. Cell suspensions were sensitized with human IgE and incubated with ketotifen fumarate or control. After antigenic challenge of sensitized cells with anti-IgE, levels of histamine and tryptase, two mast-cell granule markers, were measured in the supernatant fluid. Cell viability was assessed with a Trypan Blue assay. Ketotifen at concentrations of approximately 10(-11) to 10(-4) M inhibited mast-cell histamine release by 90% or more. Similarly, ketotifen at approximately 10(-10) to 10(-4) M inhibited tryptase release by 90% or more (apart from a single anomalous reading). At all ketotifen concentrations that stabilized mast cells, cell viability was preserved. Moreover, ketotifen did not impair cell viability unless concentrations were increased above the clinically relevant range, i.e., above the order of magnitude of 10(-4) M. These data demonstrate that ketotifen can stabilize human conjunctival mast cells, without impairing cell viability.

Anti-Allergic Agents↗
PubMed2006

Attenuation of human lung mast cell degranulation by bronchial epithelium.

BACKGROUND: Human lung mast cells (HLMC) lie in close proximity to the bronchial epithelium in asthma and adhere with high affinity to bronchial epithelial monolayers in vitro. We investigated the consequences of this adhesive interaction on HLMC activation in response to Fc epsilon RI cross-linking. METHODS: Human lung mast cells were cultured with the bronchial epithelial cell line BEAS-2B or plastic control for either 30 min or 16 h and then activated with anti-IgE. Histamine was measured by radioenzymatic assay. RESULTS: After co-culture for 30 min, IgE-dependent histamine release from HLMC was identical on both BEAS-2B and plastic. After 16 h of co-culture, there was a marked decrease in constitutive and IgE-dependent histamine release from HLMC cultured on BEAS-2B compared with those cultured on plastic or fibronectin. In contrast, the Ca(2+)/ATPase inhibitor thapsigargin produced concentration-dependent histamine release that was significantly increased on BEAS-2B compared with plastic. IgE-dependent degranulation was not significantly affected by BEAS-2B-conditioned medium. CONCLUSIONS: BEAS-2B bronchial epithelial cells attenuate IgE-dependent but not thapsigargin-induced histamine release from HLMC. The differential effect with anti-IgE compared with thapsigargin suggests that the mechanism includes interference with the proximal Fc epsilon RI signalling pathway.

Antibodies, Anti-Idiotypic↗
PubMed1991

Mast cell degranulating (MCD) peptide and its optical isomer activate GTP binding protein in rat mast cells.

The MCD peptide in bee venom induces degranulation in mast cells. The internal calcium concentration of mast cells increased and remained high following MCD stimulation. This calcium increase was blocked by pertussis toxin (Ptx) treatment, suggesting that MCD peptide activates Ptx-sensitive G-protein. Even in the absence of external calcium in the incubation medium, the calcium concentration increased by MCD treatment, but soon returned to the original level. D-MCD, the optical isomer of the MCD peptide, also increased the internal calcium concentration through a Ptx-sensitive pathway. We suggest that cationic clusters at one side of the surface are more important in activating the G-protein than the alpha-helix conformation.

Animals↗
PubMed1980

Evaluation of the role of Histamine H1- and H2-receptors in cutaneous inflammation in the guinea-pig produced by histamine and mast cell degranulation.

1 The role of histamine H1- and H2-receptors in mediating the cutaneous inflammatory response produced by exogenous histamine and the release of endogenous histamine from mast cells has been investigated by a method which permits simultaneous, quantitative measurement of vasodilatation, vascular permeability and oedema formation. 2 Histamine and the selective H1-receptor agonist, 2-(2-aminoethyl) pyridine, both produced vasodilatation, increased vascular permeability and oedema formation whereas the selective H2-receptor agonist, dimaprit, produced only vasodilatation. 3 Mepyramine and cimetidine both reduced the vasodilatation response to histamine, the combination of antagonists being superior to either antagonist alone. Mepyramine (but not cimetidine) virtually abolished extravascular albumin accumulation and oedema formation. 4 Mepyramine and cimetidine both reduced the vasodilatation response produced by active cutaneous anaphylaxis and compound 48/80. However, mepyramine was less effective in reducing the vascular permeability response to mast cell degranulation than to histamine. 5 In conclusion, the vasodilator response to histamine is mediated by both H1- and H2-receptors; the permeability response to histamine is mediated solely by H1-receptors. A combination of H1- and H2-receptor antagonists appears to be more effective than either antagonist alone in reducing cutaneous inflammatory reactions involving histamine.

Animals↗
PubMed1989

Mechanism of induction of long term potentiation by the mast cell degranulating peptide.

The properties of Long Term Potentiation (LTP), which is a sustained enhancement of the synaptic response produced by a brief train of electrical stimulation, and its mechanisms are briefly reviewed. Bath application of the mast cell degranulating peptide (MCD) - a peptide isolated from bee venom- also produces in hippocampal slices LTP which is indistinguishable from that produced by a train of electrical stimulation (no change in postsynaptic cell properties, APV sensitive). In vivo push-pull experiments indicate that this LTP is not associated with a sustained enhancement of release of glutamate and aspartate, the two principle transmitters of the hippocampus, but there is a delayed enhanced release of proteins in the extracellular space which may contribute to the maintenance of the potentiation.

Electric Stimulation↗
PubMed1994

Intracellular mediators of goblet cell degranulation in isolated pancreatic ducts.

The involvement of particular intracellular signalling pathways in agonist-evoked degranulation of guinea pig pancreatic duct goblet cells was investigated. Carbachol, vasoactive intestinal peptide (VIP), calcium ionophore A23187, phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), cyclic AMP analogue Sp-5,6-DCl-cBIMPS and forskolin each caused degranulation of goblet cells in isolated ducts. Degranulation induced by carbachol was not inhibited by okadaic acid, cytochalasin-D or nocodazole. These results indicate that at least two major signalling pathways are involved in pancreatic duct goblet cell secretion.

Animals↗