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PubMed1998

Metal ion-induced toxic histamine release from human basophils and mast cells.

Recent data suggest that distinct metal ions can be released from dental alloys or other biomaterials, and may cause toxic effects on various cells. In this study, the effects of 14 metal ions on histamine release from human blood basophils (n = 4), isolated tissue mast cells (lung n = 8, uterus n = 2, skin n = 1, gingiva n = 1), the basophil cell line KU-812, and the mast cell line HMC-1 were analyzed. Of the 14 metal ions, Ag+ (0.33 mM) and Hg2+ (0.33 mM) were found to induce release of histamine in blood basophils, KU-812, mast cells, and HMC-1. The effects of Ag+ and Hg2+ were dose dependent and were observed within 60 min of incubation. In primary mast cells and basophils, AU3+ (0.33 mM) also induced histamine release, whereas no effects of Au3+ on HMC-1 or KU-812 cells were seen. The other metal ions showed no effects on primary or immortal cells within 60 min. However, Pt4+ (0.33 mM) induced histamine liberation in HMC-1 and lung mast cells after 12 h. The Ag+- and Hg2+-induced rapid release of histamine from HMC-1 was associated with ultrastructural signs of necrosis, but not apoptosis. In contrast, prolonged exposure to Pt4+ (0.33 mM, 14 h) induced apoptotic cell death in HMC-1 cells, as assessed by electron microscopy and DNA analysis. Together, certain metal ions induce distinct cytopathogenic effects in mast cells and basophils. Whereas Ag+, Hg2+, and Au3+ cause direct toxicity, Pt4 causes cell death through induction of apoptosis. Whether such effects contribute to local adverse reactions to metal-containing biomaterials in vivo remains to be determined.

Basophils↗
PubMed1990

[The role of different microorganisms and infectious processes in the occurrence and course of bronchial asthma].

The role of infection in bronchial asthma (BA) is unknown. The pathogenesis of BA contributes to the origin of infectious processes induced by different microorganisms. In view of the predominance of associations of viruses and bacteria in the etiology and pathogenesis of acute respiratory infections, it is difficult to define in vivo the share and role of these microorganisms which participate in the origin and enhancement of hypersensitivity, hyperreactivity and alterations in beta-adrenoreactivity. Some factors of bacterial pathogenicity promote BA progress. On contact with basophils and mast cells bacteria (both pathogenic ones and ordinary commensals) are capable of liberating histamine and other mediators during colonization of the bronchial tree and origin other infectious process. This mechanism of mediator liberation may contribute to the transformation of pre-asthma to BA or provoke its exacerbation.

Asthma↗
PubMed1978

[Vasomotor rhinitis and vasomotor tests (author's transl)].

The classification of types of vasomotor rhinitis remains controversial. Too frequently, the presence of salvoes of sneezing leads to a diagnosis of allergy. The authors point out the only relatively accuracy of skin tests and show that marked local histamine liberation may occur in the absence of allergy. They have perfected a battery of vasomotor tests using nicotinic acid, histamine, 48/80 and acetylcholine. On this basis, they propose a pragmatic clinical classification of types of vasomotor rhinitis. Underlying tendency to tetany is the most common aetiology, going hand in hand with increased histamine sensitivity.

Acetylcholine↗
PubMed1982

Species and tissue differences of histamine storage and release.

Histamine release by compound 48/80 was studied in vivo and in vitro in different tissues of the cat and rat. A good correlation was fond between both kinds of experiment. The histamine stores in the cat salivary gland are poorly sensitive to this histamine-liberating substance. In vitro studies with heart and lungs of the rat and guinea pig showed no correlation between the spontaneous histamine release and the release induced by compound 48/80. This finding suggests the existence of two pools of tissue histamine, both with different storage and release properties, and most probably with different functions in the body.

Animals↗
PubMed1977

A simplified method for measuring basophil histamine release and blocking antibodies in hay fever patients. Basophil histamine content and cell preservation.

A simplified method for measuring basophil histamine release in grass pollen hay fever patients has been developed. Leukocytes were challenged in vitro with extracts of Phleum pratense (timothy) and the release of histamine was determined indirectly as the residual histamine in the cell sediment. Several steps to purify histamine thus became superfluous and histamine was directly conjugated with o-phthaldialdehyde to form a fluorophore. The simplified method showed a basophil histamine content which was in accordance with results obtained by more specific methods. No difference in basophil histamine content was found between normal and allergic persons. For the histamine liberation assay blood could be adequately preserved for transport for 48 h at room temperature by adding cell culture medium. Basophil histamine release technique allows evaluation of cell sensitivity for determination of the degree of allergy as well as the level of blocking antibodies.

Adult↗
PubMed1986

Histaminoid response after intradermal and intravenous administration of atracurium, vecuronium and tubocurarine: a comparative study.

The object of this study was to investigate the histaminoid responses after intradermal administration of atracurium, vecuronium and tubocurarine and to compare these with the cutaneous and cardiovascular responses to intravenous administration of the above relaxants in the same patients. Positive local cutaneous responses to intradermal injection were most common after tubocurarine (92%) and least common after vecuronium (12%). Tubocurarine produced the greatest fall in systolic pressure 3 min after intravenous administration but there was no difference in this respect between atracurium and vecuronium. In any individual patient the response to intradermal injection of a relaxant was not a reliable predictor of the response to subsequent intravenous administration of the same relaxant. Twenty patients had plasma IgE levels below 12 IU ml-1. This abnormally low titre occurred more frequently in female patients and was associated with an increase in the incidence and degree of histaminoid responses to atracurium and tubocurarine. Low plasma IgE may be associated with a deficiency in surface IgE on mast cells which therefore have an increased sensitivity to drugs that cause direct pharmacological histamine liberation.

Adolescent↗
PubMed1998

Effects of dental amalgam and its components of histamine release from human basophils and tissue mast cells.

Recent studies have shown that metal ions can be released from dental amalgam or other dental materials, and can cause toxic effects on various cells. In this study, the effects of amalgam-conditioned culture medium (ACCM), components of amalgam (Ag+, Cu2+, Sn2+, Hg2+) and dental composite-conditioned culture medium (CCCM) on histamine release from human blood basophils (healthy subjects, n = 3) and tissue mast cells (n = 3) were analyzed. ACCM and CCCM were prepared using either fresh or 6-weeks-aged specimens. Of the metal ions tested, Ag+, and Hg2+ were found to induce histamine release from basophils (Ag+, 0.33 mM: 83 +/- 11% vs Hg2+, 0.33 mM: 100% vs control medium: 5 +/- 5%) and mast cells (Ag+, 0.33 mM: 91 +/- 16% vs Hg2+, 0.33 mM: 99 +/- 1% vs control: 2 +/- 1%), whereas no effects were seen with Cu2+ and Sn2+. Neither ACCM from freshly prepared amalgam nor ACCM from 6-weeks aged amalgam, produced histamine release in basophils or mast cells. Inductively coupled plasma atomic emission spectrometry (ICP) revealed that the Ag(+)- and Hg(2+)-concentrations in ACCM were below the range in which histamine release occurred. Similar to ACCM, no effects on basophils or mast cells were observed with CCCM. In summary, our data show that distinct metal ions present in dental amalgam, can induce (toxic) histamine liberation from basophils and mast cells. However, the amounts of metal ions released from amalgam apparently were too low, to cause histamine release.

Basophils↗
PubMed1998

[An attempt to block histamine release from basophils granulocytes with antibodies obtained as a result of long-term immunization].

UNLABELLED: Pathogenetic mechanisms responsible for efficacy of specific immunotherapy still remain to be fully explained. This concerns both desensitization with classic allergens and very rarely used specific immunotherapy with bacteria. Microbes can play important role as hypersensitivity factor in some allergo-inflammatory processes. Bacterial products may act as basophil histamine liberators through immunological (IgE-mediated) and nonimmunological--particular lectin-sugar way. The aim of study was to verify if histamine release triggered by microbes could be modified (blocked) with specific antibacterial antibodies--taking into consideration both of mechanisms of basophil degranulation. The size of immediate (in healthy persons--Tab. 3, 4) and late as well as delayed (in asthmatic patients--Tab. 8) skin reactivity to examined microorganisms and the degree of basophil histamine release induced with these bacteria were compared. Human basophils were isolated from peripheral blood on Ficoll-Hypaque gradient, next challenged with whole, formalin-killed bacteria and with the same bacteria after incubation with specific and nonspecific sera. To differentiate between IgE-dependent and non-immunological mechanisms of histamine release, the IgE molecules were removed from the surface of the basophils by exposure to pH 3.6 (stripping). In each experiment histamine release induced by anti-IgE antibodies was used as control of stripping (Tab. 5, 9). Levels of histamine from the basophils (without and after stripping) incubated with non-coated and specific antibodies coated bacteria were compared. The results were expressed as a percentage of total histamine content in the sample. Histamine release was assayed spectrofluorometrically by using Shore method in Norn modification. The main investigations concerned the basophils from 12 healthy, non-atopic individuals, who had positive immediate skin reactions with at least 1 from 3 microbial strains: Staphylococcus aureus 9615 (unencapsulated), Staphylococcus aureus Smith (encapsulated) and Escherichia coli. Sera containing specific antibodies for these microorganisms were obtained from immunized rabbits. As negative control served sera collected from animals after immunization. Additionally the basophils of 6 asthmatic (intrinsic asthma) patients treated with autovaccines were examined. All patients demonstrated positive late and delayed skin reactions, 3 of them also immediate, to autologous Neisseria and Moraxella species cultured from upper respiratory tract. The bacteria were used as a component of autovaccine and as a basophils stimulating factor in histamine assay. Microbes were incubated with patients own sera before (unspecific serum) and after treatment (source of "specific" antibodies). CONCLUSIONS: 1. Bacteria induced basophil histamine release through two ways: immunological (IgE-mediated) and non-immunological (sugar-lectin interactions). 2. Non-immunological interactions played the main role in basophil histamine release induced by bacteria--both in normal individuals and asthmatic patients. 3. Sera of immunized with bacteria animals partially reduced basophil histamine release induced by homologous strains (Tab. 7). 4. An incubation of autologous bacterial strains with asthmatic patients's sera collected after autovaccines treatment has no influence on basophil histamine release induced by these microbes (Tab. 9). 5. There was no correlation between the skin reactivity to bacteria (both in healthy persons and in asthmatic patients) and the intensity of basophil histamine release induced by microbes.

Adult↗
PubMed1987

Potassium-induced histamine release from mast cells and its inhibition by ketotifen.

Potassium chloride induced a dose-dependent release of histamine from rat peritoneal mast cells at concentrations from 5 to 150 mM in the absence of extracellular Ca2+. Potassium concentrations greater than 150 mM produced less histamine release. The release was energy-dependent and was complete within one minute. The histamine liberating effect of KCl could be inhibited by NaCl and by preincubation with ketotifen. The monovalent cations, Rb+ and Cs+ also evoked histamine release, whereas Na+ and Li+ were ineffective.

Animals↗
PubMed1988

Effect of antianaphylactic agents on substance-P induced histamine release from rat peritoneal mast cells.

Substance P is known to be a potent histamine liberator for mast cells. The influence of antianaphylactic agents, disodium cromoglycate (DSCG), ketotifen, and tranilast was studied on substance-P and compound 48/80-induced histamine release from rat peritoneal mast cells. Substance-P induced histamine release was inhibited by these agents, while compound 48/80-induced histamine release was not inhibited by tranilast. Our findings suggest that these antianaphylactic agents are assumed to be effective for cutaneous diseases which might be concerned with substance P and histamine.

Animals↗
PubMed1971

Electron microscope observations on compounds 48-80-induced degranulation in rat mast cells. Evidence for sequential exocytosis of storage granules.

In vitro degranulation of rat mast cells was studied at different intervals ranging from 10 to 60 sec after adding the histamine liberator, compound 48/80 (0.4 microg/ml, 17 degrees C). The ultrastructural changes were followed by electron microscopy, and parallel assays were made to determine the histamine released. In addition, the extracellular tracers lanthanum and hemoglobin (demonstrated by its peroxidative activity) were applied to mast cells to follow communication of the extracellular space with the cavities formed during degranulation. After a lag period of 10 sec, degranulation started in the most peripherally located granules. The perigranular membrane fused with the plasma membrane, resulting in a pore bridged by a thin diaphragm. This was followed by rupture of the diaphragm and extrusion of the granule matrix (exocytosis). The process advanced towards the cell interior by fusion and opening of the deeper situated granules to the formerly opened granule cavities. At the end of the process, the cell was filled by a system of complicated cavities containing a number of altered granules. Extracellular tracers have shown that these intracellular cavities were in unbroken communication with the extracellular space from the very beginning of their formation. Both lanthanum and hemoglobin were found to be adsorbed to the limiting membrane of the cavities and bound to altered mast cell granules. In contrast, no tracer substance was present in nondegranulating mast cells. Degranulation of mast cells by compound 48/80 is regarded as a sequential exocytosis, a process similar to that described for some exocrine gland cells. All the "intracellular" cavities, formed by degranulation, were shown to communicate with the extracellular space; consequently, granules lying in these cavities must be considered as biologically extracellular. The present findings support the view that histamine is released from the granule matrix by the extracellular ionic milieu.

Animals↗
PubMed1979

Enigma of disodium cromoglycate action on mast cells.

In rat peritoneal mast cells, disodium cromoglycate showed no inhibitory effect on histamine release values if the cells were preincubated with the drug for 40 min prior to stimulation with antigen, compound 48/80 or ATP. If the drug was added simultaneously with antigen or a low dose of compound 48/80, a repression of histamine release occurred. No such effect was noted if ATP was employed as histamine liberator.

Adenosine Triphosphate↗
PubMed1981

Allergic contact dermatitis of the mouse ear.

Allergic contact dermatitis to picryl chloride on the mouse ear was registered by measuring the increasing wet weight during the inflammatory reaction. This quantitative technique permitted the use of small experimental groups of regular laboratory mice. Full sensitization to picryl chloride is achieved as early as 3 days after a single painting with the hapten. The allergic reaction peaks at 24 h after challenge. Sensitization and challenge are not inhibited, whether by antihistamine, histamine liberator, or antiserotonin. The hypersensitivity state lasts at least 4 months.

Animals↗
PubMed1968

The actions of caerulein on gastric secretion of the dog and the rat.

1. Caerulein, as expected from its amino-acid composition and sequence, has a potent stimulant action on gastric secretion in the dog, the rat and the frog.2. In the denervated fundic pouch of the dog, caerulein increases the rate of flow of gastric juice and the outputs of acid and pepsin. Acid concentration and pepsin concentration in caerulein-produced juice are generally greater than in control juice. The threshold subcutaneous dose of caerulein is 0.15-0.5 mug/kg and the threshold rate of intravenous infusion 0.25-0.5 mug/kg per hr. Rapid intravenous injection is ineffective. On a molar basis, caerulein is approximately twice as active as human gastrin I on volume and acid output of the gastric pouch and 4 times as active on pepsin output.3. Sustained acid secretion of the fundic pouch produced by histamine infusion is inhibited by caerulein, administered either intravenously or subcutaneously. In turn, acid secretion elicited by caerulein is inhibited by atropine.4. In the rat, the activity ratio of caerulein to human gastrin I is 7-30, calculated on a molar basis, and is thus considerably greater than in the dog. Further, caerulein is 3 times more active than cholecystokinin-pancreozymin. Tested on the perfused stomach preparation of the rat, the threshold dose of caerulein by rapid intravenous injection is 25 ng/kg, by intravenous infusion 0.25 mug/kg per hr, and by subcutaneous injection 0.25 to 0.5 mug/kg.5. The activity of caerulein is sharply reduced by pretreatment of the rats with the histamine liberator 48/80 and potentiated by pretreatment with the diamine oxidase inhibitor aminoguanidine. When caerulein is given by rapid intravenous injection during a priming infusion of histamine its effect is enhanced and considerably prolonged.6. The isolated mucosa of the frog stomach is extremely sensitive to caerulein which, in a concentration of a few pg/ml., stimulates active transport of chloride.7. Qualitative and quantitative differences in the action of gastrin and caerulein are pointed out, and particular emphasis is laid on the importance of esterification of the tyrosyl residue for the biological activity of caerulein.

Animals↗
PubMedDate not supplied

The possibility of passive transport of histamine through biological membranes.

The possibility of transport of free and heparin-bound histamine along the concentration gradient through bimolecular lipid membranes (BLM) and the influence of various factors on it was studied. It was shown that histamine is capable of diffusing through BLM in the form of a singly charged cation. In contrast to histamine, neither heparin nor the histamine-heparin complex (HsHC) penetrates through BLM. It was established that the action of histamine-liberating factors -- increasing the ionic strength to 0.15 and the addition of trypsin to the solution -- on HsHC leads to the appearance of transport of histamine through the BLM as a result of an increase in the concentration of free histamine in solution.

Biological Transport↗
PubMed1983

Effect of a single UVB or PUVA exposure on immediate and delayed skin hypersensitivity reactions in humans. Correlation to erythemal response and Langerhans cell depletion.

A single UVB or PUVA exposure given 4 days prior to skin testing affected skin responses both to contact allergens and to histamine and the histamine liberator, compound 48/80. The delayed contact hypersensitivity reactions were attenuated by UVB in 75% and by PUVA in 79% of the tests. The immediate skin reactions to histamine and compound 48/80 were diminished by UVB in 81% and by PUVA in 46% of the cases. While the epidermal Langerhans cell (LC) density was distinctly affected by irradiation, the attenuation of skin hypersensitivity reactions seemed to be independent of the degree of LC depletion. A significant correlation was, however, found between the strength of the erythemal reaction induced by the irradiation and the attenuation of the skin hypersensitivity test reactions; this was true for both delayed and immediate skin reactions in the case of UVB and for immediate skin reactions in the case of PUVA. The mechanism behind the attenuating effect of UV radiation on skin hypersensitivity reactions remains unknown, but it probably does not result from a stabilization of the mast cell membrane, as histamine and compound 48/80 induced reactions were suppressed to a similar extent.

Adult↗
PubMed2001

Effects of cold stress and epinephrine on degranulation of peritoneal mast cells in rats.

We studied the effects of histamine liberators calcium ionophore A23187 and substance 48/80 on mast cells during cold stress and epinephrine load. Under the effect of both stress factors, ionophore A23187-induced histamine release from mast cells underwent more pronounced changes than that stimulated by substance 48/80. Cold stress and epinephrine load produce different changes in functional activity of Ca2+ channels in mast cell membranes.

Animals↗
PubMed1989

The human skin mast cell.

The abundance of mast cells in human dermis, together with their ability to release a variety of vasoactive and pro-inflammatory mediators following cross-linkage of their cell-surface receptors for IgE, enables these cells to provide an effective defence mechanism within this organ. A similar defensive function is attributed to mast cells of other human organs such as intestine and lung which are in contact with the external environment and therefore susceptible to infiltration by foreign allergens and micro-organisms. However, mast cells of the skin apparently differ from those present in lung and intestine in being activated for histamine release by a variety of endogenous neuropeptides which stimulate the rapid release of histamine in the virtual absence of eicosanoids. This would provide a mechanism of neurogenic control of a variety of homeostatic functions such as blood flow, angiogenesis and fibroblast proliferation. Such processes would aid in the remodelling of tissue during wound healing, and increased numbers of mast cells have been noted around healing wounds of rat skin and areas of developing fibrosis. Neuropeptides modulate the activity of a variety of immuno-competent leucocytes including macrophages, monocytes and lymphocytes. The findings that skin mast cells are activated by neuropeptides suggest that these cells may also be included amongst those involved in neuro-immune interactions. Activation of skin mast cells by non-immunological stimuli may contribute to the aetiology of some forms of skin disease. Patients with chronic idiopathic urticaria appear to have enhanced vascular responsiveness to intradermal injections of the histamine liberator codeine suggesting that this disease may involve hyper-responsiveness of their mast cells to endogenous non-immunological stimuli. The findings of large increases in histamine accompanied by small increases in PGD2 in venous effluent of thermally challenged limbs of patients with cold- or heat-induced urticaria may suggest that their mast cells had been activated by a non-immunological stimulus. However, the interpretation of results gained using such relatively complex in-vivo systems are difficult, as the cellular origin of the detected mediators is by no means clear. However, it is hoped that in the future the alliance of newly developed in-vitro techniques to investigate mast cell function together with in-vivo methods to investigate their interaction with elements in their tissue environment will greatly increase our understanding of the role of the human skin mast cell in health and disease.

Histamine↗