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At least 19 recordsLinked to original sources
PubMed1979

Effect of synthetic cyclic nucleotides on immunologic histamine release from calf granulocytes.

Sensitized bovine granulocytes release histamine when exposed to specific antigens. A unique modulation of histamine release by adrenergic agents has been shown in the bovine; beta-adrenergic agonists enhance and alpha-adrenergic agonists inhibit histamine release. This is an opposite response to that reported in other species. The present study was undertaken to determine the possible relationship between cyclic nucleotides and adrenergic agents in this species. Dibutyryl cAMP enhanced antigen-induced histamine release over the complete concentration range tested (10(-6)--10(-3)M); it also overcame, in a dose-dependent manner, the inhibition of antigen-induced histamine release produced by 10(-4) M phenylephrine. The 8-bromo cGMP AND 0-MONOBUTYRYL CGMP had no significant effect on antigen-induced histamine release nor did 8-bromo-cGMP have any significant effect on the enhancement of histamine release produced by 10(-4) M dibutyryl cAMP. These findings suggest that only cAMP has a role in the modulation of antigen-induced histamine release from bovine granulocytes.

Animals↗
PubMed1977

Enhancement of IgE-mediated histamine release from human basophils by viruses: role of interferon.

Human leukocytes maintained in culture are induced to release histamine when exposed to ragweed antigen E or anti-IgE. Leukocyte cultures incubated with virus (i.e. HSV-1, Influenza A, and Adeno-1) but not exposed to ragweed antigen E or anti-IgE fail to release histamine. If, however, leukocyte cultures are first exposed to virus and then to ragweed antigen E or anti-IgE, significant enhancement of histamine release occurs. Both infectious and inactivated virus enhance histamine release and the degree of enhancement is related to the concentration of virus and the length of the incubation. Tissue culture fluid harvested 8 h after exposure of leukocytes to virus contains a soluble factor which is capable of enhancing histamine release when added to fresh leukocyte cultures. This factor has all the properties of interferon including species specificity and cannot be dissociated from the antiviral activity of interferon. Moreover, both known inducers of interferon (poly I:poly C) and standard preparations of interferon are capable of enhancing histamine release. The enhancement of histamine release by interferon represents a new biological role for interferon.

Adenoviridae↗
PubMed1976

Complement-induced histamine release from human basophils. II. Mechanism of the histamine release reaction.

The activation of human serum complement by incubation with zymosan generates C5a which releases histamine from autologous basophils. The characteristics of the C5a-induced histamine release were investigated. It is similar to IgE-mediated reactions in requiring Ca++ and in being inhibited by EDTA. However, it has marked differences from IgE-mediated reactions. C5a, at all concentrations, released histamine completely in less than 2 min. The C5a reaction has a narrow pH optimum that antigen-induced release and occurs well at 17 degrees to 37 degreesC but not at 0 degreesC. The optimal reaction temperature is 25 degrees to 30 degrees C. Unlike the antigen-induced release, no two-stage activation with C5a for the release of histamine could be demonstrated. There was additive release between C5a- IgE-mediated reactions. Leukocytes could be desensitized to the C5a-mediated reaction by 1) incubating the cells at 37 degrees C for 45 min, 2) pretreating the leukocytes with activated serum in the presence of EDTA, and 3) adding the activated serum to the leukocytes at 0 degrees C before transferring to the optimal reaction temperatures. Cells desensitized to the complement-induced release have normal reactions to IgE-mediated histamine release. In parallel experiments, cells from allergic donors desensitized for IgE-mediated reactions by incubation with antigen under sub-optimal conditions release histamine normally upon the addition of C5a. The results indicate that histamine release by C5a involves a mechanism of basophil activation that is different from the pathway involved in the IgE-induced reaction.

Antigens↗
PubMed1975

Mechanism of histamine release by alpha-chymotrypsin from isolated rat mast cells.

Alpha-chymotrypsin (CT) was modified chemically and physically by the treatments with diisopropyl fluorophosphate, L-(1-tosylamide-2-phenyl) ethylchloromethylketone, hydrogen peroxide and heat. After these treatments, CT lost or decreased both the enzymic activity and ability of releasing histamine from rat mast cells. Ca++ was essential for histamine release by CT, while it enhanced only slightly the enzymic activity. Process of histamine release by CT could be separated into two stages: CT-dependent but not Ca++-dependent, and Ca++-dependent but not CT-dependent. The activated state of mast cells produced by CT decayed rapidly at 37 degrees C in the absence of Ca++, but these cells responded to Ca++ by adding CT once again, suggesting reconstitution of cell membrane structure affected by CT. Isoproterenol, epinephrine, prostaglandin E1, and dibutyryl-cyclic AMP (0.01-0.1 mM) did not inhibit release of histamine induced by CT. Neither theophylline (0.01-0.1 mM) alone nor the combinations of these cyclic AMP-active agents with theophylline inhibited the release of histamine. But, in the presence of papaverine (0.01-0.1 mM) a marked, dose-dependent inhibition was observed. These data suggest that 1) release of histamine by CT from rat mast cells is causally related to its hydrolytic activity, 2) this activity causes a reversible change on mast cell membrane which probably facilitates Ca++-influx through the cell membrane, and 3) there are subtle differences among CT, compound 48/80 and antigens concerning the effect of cyclic AMP-active agents in histamine-releasing mechanisms in mast cells.

Animals↗
PubMed1976

Histamine release by chemotactic, formyl methionine-containing peptides.

Certain formyl dipeptides and tripeptides containing methionine released histamine from human basophils at concentrations of 10(-4) to 10(-7) M. However, N-formyl amino acids did not release histamine. Tripeptides, in general, were more active than dipeptides. An acyl group was required for histamine release although an N-terminal position for Met was not essential. Histamine release from human basophils by these peptides correlated well with their chemotactic activity for rabbit leukocytes.

Animals↗
PubMed1977

Mechanism of histamine release by formyl methionine-containing peptides.

Small, acylated, methionine-containing peptides release histamine from human basophils. The characteristics of this reaction were compared to that of C5a- and IgE-induced release. fMet peptide-induced release requires Ca++ and is inhibited by EDTA in a manner similar to IgE- and C5a-mediated reactions. The fMet-Phe-Met-initiated reaction is complete within 2 min at temperatures of 25, 30, and 37 degrees C; but does not occur at 0 degrees C. There was a large variation in the capacity of leukocytes from different donors to release histamine with fMet peptides. However, there was no correlation in the capacity of leukocytes to release histamine with fMet-Phe-Met and their release with C5a or anti-IgE. The release by fMet-Phe-Met (but not by C5a or anti-IgE) was reversibly inhibited by a nonreleasing tripeptide. Leukocytes could be desensitized to the action of active fMet-peptide by preincubation with the peptide in the absence of cations. After washing, these cells released normally with C5a or anti-IgE. Conversely, cells desensitized to the action of C5a- or IgE-mediated reactions released normally with fMet peptides. There was cross-desensitization between different active peptides, and inactive peptides could not desensitize the leukocytes. Pharmacologic agents had similar effects on C5a and fMet peptide-induced release (e.g., lack of enhancement with deuterium oxide; enhancement with cytochalasin B; and inhibition with aminophylline and dibutyryl cyclic AMP). Therefore, histamine release with fMet peptides is initiated by their binding to and activation of a specific receptor on the basophil; the reaction beyond that point is similar to the C5a-mediated reaction.

Complement C5↗
PubMed1977

Modulation of antigen-induced histamine release from bovine granulocytes by several anti-allergic agents.

Sensitised bovine granulocytes release histamine when exposed to antigen. Several anti-allergic agents, some previously shown to be active in cattle, were tested to investigate their modulation of this histamine release process. Diethylcarbamazine citrate potentiated release at low concentrations and inhibited at high concentrations. Sodium meclofenamate and PR-D-92-EA were potent inhibitors. Acetylsalicylic acid and ICI 74,917 inhibited at high concentrations. Disodium cromoglycate was relatively ineffective, although it potentiated histamine release at low concentrations.

Animals↗
PubMed1975

Ionophore A-23187 induced histamine release from rat mast cells and rat basophil leukemia (RBL-1) cells.

Ionophore A-23187 releases histamine from normal mast cells apparently by promoting Ca++ influx (Foreman et al, Nature 245: 249, 1973). In our hands at concentrations of greater than 0.2 mug/ml release occurs in 1 to 2 min, is blocked by metabolic inhibitors, and is unaccompanied by cytotoxicity (trypan-blue uptake, lactic dehydrogenase (LDH) release). At higher doses (0.5 mug/ml) histamine release is followed by significant cytotoxicity, but again Ca++ is required. In parallel studies, we examined cultured rat basophilic leukemia (RBL-1) cells. These cells, which apparently have normal surface receptors for IgE, contained approximately 700 ng histamine/10(6) cells but did not release histamine when IgE-mediated release was looked for. They do not respond to doses of ionophore which would be expected to give non-cytotoxic histamine release. At higher doses histamine release is preceded by progressive LDH release: LDH release is 75% complete at 5 min whereas 10 min are required for 75% maximal histamine release. This reaction requires Ca++ and is temperature dependent but is not inhibited by metabolic poisons (2-deoxyglucose, dinitrophenol, CN-). These studies suggest that either Ca++ does not enter into these cells normally or that one or more mechanisms which are ordinarily triggered by the changes in Ca++ flow are unresponsive in the RBL-1 cells. These studies also underline the importance of ruling out cytotoxicity in ionophore-induced phenomena.

Animals↗
PubMed1978

Mechanism of histamine release induced by the ionophore X537A from isolated rat mast cells.

X537A released histamine from isolated histamine-retaining mast cell granules incubated at 37 degrees C in Tris-sodium (150 mM) or Tris-potassium (150 mM), but not in Tris-glucose (300 mM). The release was depressed at 0 degrees C. In contrast, decylamine released all histamine bound to the granules irrespective of the presence of monovalent cations in the incubation medium of temperature. X537A did not release histamine from an artificial heparin-protamine complex when incubated in deionized water. The mechanism of histamine release by X537A can be explained by the ability of the ionophore to carry monovalent cations across cellular membranes, hereby making the ions available for exchange with histamine bound to the granular matrix. This mechanism can be distinguished from that of agents triggering an exchange between cations and bound histamine through a calcium- and energy-dependent exocytotic process on the one hand and through membrane lysis on the other. Based on the observation that the ionophore was able to carry histamine into the bulk of an organic phase, various possibilities exist to explain how histamine escapes from the cells following release from intracellular granular stores.

Animals↗
PubMed1975

Inability of Ni++ and Co++ to release histamine from rat peritoneal mast cells.

Ni++ and Co++ concentrations from 10 minus 3M to 10 minus 6M were added to rat peritoneal mast cells. These metal ions, at the concentrations indicated, did not cause histamine release from the mast cells, and did not inhibit the histamine release mediated by compound 48/80. On the basis of these studies, anaphylactoid edema of the rat following injection of i++ or Co++ is on a basis other than a direct effect of the m-tal ion on mast cells.

Animals↗
PubMed1977

Histamine release from human leucocytes. A serum factor necessary for the induction of histamine release and desensitization by protein A.

The ability of human leucocytes to release histamine on protein A treatment is lost when the cells are washed repeatedly. It is, however, possible to restore the sensitivity to protein A treatment by incubating the leucocytes in serum. Treatment of the cells with purified IgG does not restore the activity. The material responsible for the resensitization is eluted both in the second and the third protein peak when serum is chromatographed on Sephadex G-200, indicating the possible existence of several active factors. Material with low immunoglobulin content, but with retained capacity to resensitize leucocytes to release histamine on protein A treatment, was obtained by repeated chromatography of peak III material on the Sephadex G-200 column. Furthermore, material from the second and third peaks from Sephadex G-200 deprived of their IgG by passage through a protein A Sepharose or a DEAE-cellulose column had the same capacity to resensitize the leucocytes as unseparated material. When serum was separated by Pevikon block electrophoresis, most of the activity was detected in the alpha and beta regions but only little in the gamma region. The serum fractionations indicate that neither IgG nor the other immunoglobulins are the factor(s) responsible for resensitizing the leucocytes to release histamine on protein A treatment. Beside being necessary for protein A-induced histamine release, the factor (or factors) is also essential for protein A-induced desensitization of human leucocytes.

Bacterial Proteins↗
PubMed1979

On the mechanism of histamine release induced by thapsigargin from Thapsia garganica L.

Thapsigargin (Tg) is a pure chemical compound isolated from Thapsia garganica with a molecular weight of 650. It releases histamine from isolated rat mast cells but not from isolated histamine-retaining mast cell granules. The rate of release is markedly influenced by pretreatment of mast cells with Tg prior to the addition of calcium. In agreement with the effect of the ionophore A23187 but in contrast to many other calcium-dependent histamine-releasing agents, cells preincubated with Tg respond to the secretory action of calcium whenever the ion is introduced. However, after dilution of Tg-pretreated cells histamine release induced by the addition of calcium became dependent on the time of its addition. The secretory reaction induced by Tg and calcium can be divided into a two-step reaction at 37 degrees C. Pretreatment of mass cells with Tg renders the cells insensitive to the secretory action of compound 48/80 in the absence of calcium, and this effect could be partly counteracted if 1 mM of strontium was added together with compound 48/80. It is concluded that among various calcium- and energy-dependent histamine-releasing agents Tg most closely resembles the action of fluoride on isolated rat mast cells.

Animals↗
PubMed1979

Inhibition of rat mast cell degranulation and histamine release by histamine-rat gammaglobulin conjugate.

Histamin-rat-gamma-globulin conjugate inhibited degranulation and histamine release of rat peritoneal mast cells to a greater extent than the rat globulin or histamine alone. Since mast cells contain histamine receptors, it may be assumed that the histamine bound to the gamma-globulin combines with the rat mast cell histamine receptor and inhibits the degranulation and histamine release by a feedback mechanism.

Animals↗
PubMed1975

Effects of adenosine-5'-triphosphate (ATP) on rat mast cells: influence on anaphylactic and compound 48/80-induced histamine release.

Anaphylactic histamine release from mast cells isolated from actively sensitized rats was inhibited by pre-incubation with micromolar concentrations of ATP. The inhibition was reversible under various experimental conditions and was counteracted by the presence of calcium in the incubation medium. Histamine release induced by compound 48/80 was similarly affected. Mast cells exposed to antigen under conditions when histamine release was inhibited by ATP became desensitized. The results indicate that ATP inhibits the release mechanism at a step which occurs after the binding of antigen to IgE.

Adenosine Triphosphate↗
PubMed1977

Complement-induced histamine release from human basophils. III. Effect of pharmacologic agents.

Human serum activated with zymosan generates a factor (C5a) that releases histamine from autologous basophils. Previously we have presented evidence that this mechanism for C5a-induced release differs from IgE-mediated reactions. The effect of several pharmacologic agents known to alter IgE-mediated release was studied to determine whether they have a similar action on serum-induced release. Deuterium oxide (D2O), which enhances allergic release, inhibited in a concentration-dependent fashion the serum-induced reaction at incubation temperatures of 25 and 32 degrees C. The colchicine-induced inhibition was not reversed by D2O. Cytochalasin B, which gives a variable enhancement of IgE-mediated release, had a marked enhancing effect on the serum-induced reaction in all subjects tested. The following agents known to inhibit the IgE-mediated reaction also inhibited serum-induced release at 25 degrees C: colchicine, dibutyryl cyclic AMP, aminophylline, isoproterenol, cholera toxin, chlorphenesin, diethylcarbamazine, and 2-deoxy-D-glucose. These results suggest that the serum-induced release is modulated by intracellular cyclic AMP, requires energy, and is enhanced by the disruption of microfilaments. The lack of an effect by D2O would suggest that microtubular stabilization is not required. The data can be interpreted to indicate that IgE- and C5a-mediated reactions diverge at a late stage in the histamine release pathway.

Aminophylline↗
PubMed1979

Synthetic peptides comprising sequences of the human immunoglobulin E heavy chain capable of releasing histamine.

On the basis of previous studies on the structure-activity relationship of model polypeptide histamine liberators, a site within the Fc region of immunoglobulin E antibody molecules has been proposed as that responsible for the direct triggering of target mast cells after antigen challenge. Peptides comprising this region of the epsilon-chain have now been synthesized and shown to induce histamine release from normal rat peritoneal mast cells in a selective manner essentially similar to that mediated by anaphylactic antibody-antigen interaction.

Animals↗