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PubMed1975

Complement-induced histamine release from human basophils. I. Generation of activity in human serum.

The incubation of zymosan, endotoxin, or immune aggregates with normal human serum activates a factor which induces release of histamine from autologous basophils. The reaction can be divided into two steps: in the first, complement must be activated and in the second, the histamine-releasing factor interacts with basophils. The generation of histamine-releasing activity in serum occurs at 17 to 37 degrees C but not at 0 degrees C, is inhibited by heating the serum at 56 degrees C for 30 min, or by the addition of EDTA to the serum. Once generated, the histamine-liberating activity is stable to heating at 56 degrees C for 30 min. Gel filtration of the activated serum demonstrated that this factor eluted in the same region as a factor with chemotactic activity. Both factors have a molecular weight of about 16,000 daltons and their activities were inhibited by antibody to human C5. This is therefore a pathway for histamine release by C5a where the activation of the basophil is unrelated to the membrane bound IgE.

Animals↗

PubMed1975

[Basophil leucocytes and hyperlipidemia (author's transl)].

In explorations with 42 patients, who have got 2 g of fat per kg body weight, Heidsick, a member of our hospital, discussed quantitative and qualitative changing in basophil leucocytes in relation to the cholesterol and triglyceride content of the blood and the body weight. He showed, that there was an increase of basophil leucocytes under the load of fat and a changing in their cellular structure. There was no significant relation to the cholesterol level in blood, but there was such one in a group of healthy persons to the triglyceride level. Important was also a significant correlation between the body weight and the number of basophilic leucocytes.

Adult↗

PubMed1979

Characterization of the IgE receptor isolated from human basophils.

The IgE receptor of human basophils was purified by using simple and repetitive affinity chromatography on human IgE-Sepharose. Basophils were partially purified from peripheral blood of patients with chronic myelogenous or basophilic leukemia. Cells were labeled with 125I by using the lactoperoxidase method and were solubilized with nonionic detergent. Elution of IgE-Sepharose with 0.5 N acetic acid, 1% NP-40 allowed recovery of active IgE receptor. Analysis of human IgE receptor by SDS polyacrylamide gel electrophoresis with 10% gels demonstrated one major radioactive peak with an apparent m.w. of 58,000 to 68,000, somewhat larger than rat IgE receptor. The purified human IgE receptor was active since approximately 10 to 42% of labeled receptor could specifically rebind to insolubilized human IgE. Rebinding was blocked by nanomolar concentrations of soluble human IgE or rat IgE but not by human or rat IgG, heat-inactivated human IgE, or heat-aggregated human IgG; thus it appears that rat IgE receptor. The relative abilities of active rat IgE and active human IgE to inhibit human IgE receptor rebinding could not be precisely determined because of the limitations in assessing the proportion of human IgE that retains receptor-binding activity.

Animals↗

PubMed1975

Intravascular effects of IgE antibody upon basophils,, neutrophils, platelets and blood coagulation in the rabbit.

Rabbits synthesizing only IgE antibody to BSA were challenged intravenously with 50 mg BSA and the associated blood cell and coagulation alterations were examined. Basophils decreased by 90% within 1 min of challenge. This was followed by a 70% decrease in neutrophils and a 50% decrease in platelets by 15 min. These changes were found to be highly significant when compared to control unimmunized rabbits similarly challenged. By 60 min, the neutrophils and platelets in the experimental rabbits had returned to 50 and 80% of their prechallenge levels respectively, but no basophils were demonstrable by toluidine blue staining. Lymphocyte counts in the experimental rabbits did not differ from controls at 0, 1, 15, or 60 min after challenge. Blood coagulation alterations also occurred after BSA challenge in the rabbits synthesizing IgE. A significant shortening of the whole blood clotting time in plastic tubes at 25 degrees C occurred in blood samples taken at 30 sec after antigen challenge. Similarly, in vitro addition of BSA to blood samples taken prior to challenge significantly shortened the whole blood clotting time. In addition, significant prolongation of whole blood clotting times was observed in blood obtained 60 min after challenge, but only among the rabbits positive for systemic anaphylaxis. This in vivo study corroborated the known in vitro effects of IgE upon the rabbit blood basophil and platelet. In addition, the results indicate that the intravascular interaction of antigen with specific IgE antibody induced neutrophil and blood coagulation alterations.

Animals↗

PubMed1975

Basophilic leucocytes: structure, function and role in disease.

We have attempted to review the current state of our knowledge concerning the human basophilic leucocyte, drawing on experimental data derived from animals when necessary. Long neglected, a great deal has been learned about these cells in recent years, about their morphology, their biochemical constitutents and their ability to synthesize certain of these constitutents, their interactions with homocytotropic antibodies, their release of mediators in anaphylaxis, their response to chemotatic stimuli, their participation and progressive degranulation in cell-mediated hypersensitivity reactions, and their capacity for ingesting and releasing certain exogenous tracers. Despite this vast accumulation of new information, much more must be learned before we can confidently describe the role of basophils, or of the closely related mast cells, in health or disease. It seems most unlikely that either cell exists for the purpose of destroying the organism in anaphylactic shock. Nonetheless, it is highly probably that basophil/mast cell function is closely related to the potent chemicals stored within their cytoplasmic granules. One likely possibility holds that small amounts of these chemicals are required for homeostasis (e.g., for regulation of the tone of the microvasculature) and that these cells function by releasing such substances continuously, as they are needed, in small aliquots rather than by explosive discharge. This hypothesis requires that basophils be capable of releasing their contents in piecemeal fashion. Such gradual release apparently occurs in delayed-type hypersensitivity reactions, but the mechanisms responsible for this form of degranulation have not yet been identified. This hypothesis also requires that physiological, rather than pharmacological, roles be found for histamine, heparin and possibly for other components of the basophils/mast cell granules. Progress in this direction has been extremely slow.

Animals↗

PubMed1976

Complement-mediated release of histamine from human basophils. II. Biochemical characterization of the reaction.

Release of histamine from human basophils was induced by activation of complement using zymosan. The histamine-releasing factor resembled C5a on the basis of m.w. (15,000) as well as previous studies showing inactivation by anti-C5. Complement-induced release of histamine was compared with allergic release of histamine which is mediated through appropriate allergens and reaginic IgE. Previously we demonstrated that the former reaction occurred more quickly. Both reactions were inhibited by drugs which increase intracellular concentrations of cAMP3 (theophylline, prostaglandin E1, and histamine) or which mimic the action of cAMP (its dibutyrly derivative). Calcium was required for complement-mediated release of histamine and an increasing response was observed up to physiologic concentrations (2 mM). Magnesium (0 to 1 mM) did not affect the amount of histamine released. Also, glycolysis was probably required for optimal release by complement, since both 2-deoxyglucose and iodoacetamide were inhibitory. When basophils were partly enriched by depletion of neutrophils and eosinophils, the percentage of histamine released by complement was unchanged. Finally, it was shown that activated complement desensitized basophils from responding to a second challenge by the same stimulus. Cross-desensitization was not observed between complement and pollen allergens.

Basophils↗

PubMed1980

A linear correlation between histamine release and degranulation of human basophils by specific antigen or the ionophore A23187.

Simultaneous kinetic measurements have been made of basophil degranulation and of histamine release. Both antigen and ionophore A23187 were studied. Cells from the same donor under the same conditions undergo both reactions at a similar rate. Regression analysis indicated a statistically highly significant correlation between these two parameters for activation by either antigen or ionophore. In addition, the mean slope of the regression lines approached unity indicating a close direct correspondence between the number of cells degranulated and the quantity of histamine released. At any time during histamine release almost all of the cells identifiable as basophils were confluently stained and only rarely were partly degranulated cells observed. These results suggest that: (1) histamine release is not synchronous for populations of basophils; (2) individual cells are fully activated to begin histamine release at different times during the release period and then release all or almost all of their histamine in a short time relative to the total release period; (3) some cells release essentially none of their histamine and the number of these cells varies among donors and experimental conditions accounting in large measure for the incompleteness of histamine release.

Anti-Bacterial Agents↗

PubMed1980

A comparative study on basophil histamine release and skin testing in children with allergic rhinitis.

Skin tests and histamine release from basophils induced by the same allergens in children with allergic rhinitis were compared. A qualitative correlation between these two tests was found. Basophil histamine release either spontaneous or allergen-induced during the period of developed allergic symptoms was markedly higher as compared with that in a period of clinical remission. It is concluded that basophil histamine release might be a valuable diagnostic method for detection of allergen(s) responsible for symptoms of allergic rhinitis.

Adolescent↗

PubMed1981

Influence of anions, cations and osmolarity on IgE-mediated histamine release from human basophils.

Allergen-activated human basophils require Ca2+ for the in vitro release of histamine. This study evaluated the importance of anions, cations and osmotic pressure on histamine release from human basophils. All media contained 1 mM Ca2+ and various salts or sugars were used to replace the NaCl-KCl of the control medium. Permeant anions supported release of histamine with the following order of activities: acetate - greater than Br-, I-, greater than Cl- greater than SO42-. When monovalent cations of the standard medium were replaced, RbCl, CsCl, KCl or NaCl gave results identical to the NaCl-KCl control medium; choline chloride usually enhanced while LiCl inhibited release. Finally, when sugar solutions were used to replace monovalent anions and cations of the standard medium: mannitol, lactose, sucrose, sorbitol, fructose and glucose each supported histamine release. Increasing the osmolarity of the medium by adding additional NaCl-KCl enhanced the ability of suboptimal concentrations of ragweed antigen E or anti-IgE to activate and to release histamine from leucocytes. The results indicate that histamine from leucocytes. The results indicate that histamine release from basophils requires only Ca2+ and do not support the "chemiosmotic swelling' hypothesis of secretion for these cells.

Anions↗

PubMed1982

Inhibition of basophil histamine release by anti-inflammatory steroids. II. Studies on the mechanism of action.

The glucocorticosteroids inhibit the IgE-dependent release of histamine by human basophils with an order of potency that very closely parallels that found in vivo (i.e., triamcinolone acetonide greater than dexamethasone greater than beta-methasone greater than prednisolone greater than hydrocortisone much greater than progesterone approximately tetrahydrocortisone approximately 0). The effect is seen after a 24-hr preincubation with nanomolar to micromolar concentrations of glucocorticoid. In contrast, release of histamine stimulated by the formyl methionine containing peptide f-met-leu-phe, the calcium ionophore A23187, and the tumor-promoting phorbol diester 12-O-tetradecanoylphorbol-13-acetate was not inhibited by 24-hr incubation with the potent glucocorticoid dexamethasone. Dexamethasone inhibited anti-IgE-induced histamine release without altering its rate, suggesting that the glucocorticoids do not inhibit histamine release by elevating the intracellular level of cAMP. Dexamethasone did not consistently alter either the total or occupied basophil IgE Fc receptor number, and therefore the glucocorticoid effect does not appear to be due to the modulation of cell surface Fc epsilon receptor content. These data indicate that steroid hormones inhibit basophil IgE-dependent activation through a specific glucocorticoid receptor. The mechanism by which they do so appears not to involve an elevation of cAMP or a shedding of cell surface Fc epsilon receptors. Further, because the glucocorticoids did not inhibit release initiated by the PLA2-dependent stimuli f-met-leu-phe, A23187 and TPA, the inactivation of IgE-dependent histamine release by glucocorticoids may not be the result of PLA2 inhibition.

Anti-Inflammatory Agents↗

PubMed1982

H2 antihistamines augment antigen-induced histamine release from human basophils in vitro.

H2 antihistamines, including cimetidine, burimamide, metiamide, and tiotidine, consistently augmented antigen-induced histamine release from human basophils in vitro when control histamine release was less than 20% of total. This effect was specific to the H2-receptor blocking activity of these drugs: equivalent degrees of receptor blockade by four different H2 antihistamines resulted in equipotent enhancement; H1-receptor antagonists did not alter histamine release; and aminoguanidine and amodiaquine, agents that inhibit histamine metabolism but do not block H2 receptors, did not enhance histamine release. Cimetidine did not enhance release when present a) when basophils were "activated" but did not release histamine ("first stage"), or b) when basophils were no longer susceptible to histamine inhibition ("second stage"). Thus, H2 antagonists enhanced histamine release by blocking the capacity of released histamine to act on H2 receptors to inhibit release. Because it is likely that only small percentages of histamine are released in vivo, it is possible that H2 antihistamines amplify the inflammatory process by blocking the inhibitory effects of the released histamine.

Amodiaquine↗

PubMed1983

Interferon increases IgE binding to basophils.

One of the pivotal manifestations of immediate type hypersensitivity is mediator release from a variety of mediator cells, e.g., mast cells and basophils. The essential step of this process is the binding of immunoglobulin E (IgE) to the surface of these cells. In the present studies we examined the influence of human interferon (HuIFN) on the binding of IgE to human leukocytes (basophils). The results of these studies indicate that pre-treatment of leukocytes (basophils) with different types of IFN leads to a pronounced increase in binding of IgE to these cells. These data support the hypothesis concerning a pathogenetic role of IFN in the development of allergy of the immediate type hypersensitivity.

Basophils↗

PubMed1984

Effect of prostaglandin D2 in modulating histamine release from human basophils.

Prostaglandin (PG) D2 is the major cyclooxygenase metabolite of arachidonic acid released after immunologic stimulation of mast cells. In this report, we demonstrate that this PG is unlike other PGs previously investigated in that it enhances human basophil histamine release at concentrations of 1 to 100 nM. Enhancement is seen when antigen, the phorbol diester, 12-O-tetradecanoylphorbol-13-acetate and ionophore A23187 are used to initiate release and, in preparations of basophils, purified to 51 to 66% of total cell number as well as in preparations of mixed leukocytes. This enhancement is a late or "second stage" phenomenon as defined by the two stages of histamine release and is additive with the enhancement produced by D2O, but not with the enhancement produced by indomethacin or 5-hydroperoxyeicosatetraenoic acid. PGD2 also reverses the inhibition of release produced by drugs and hormones such as dimaprit and PGE2 that activate adenylate cyclase to increase cellular cyclic AMP levels. These data suggest that PGD2 may play an important role in allergic and immunologic reactions and suggest a mechanism by which mast cells and basophils can interact during these reactions.

Arachidonic Acids↗

PubMed1984

Synthesis of surface immunoglobulin E receptor in Xenopus oocytes by translation of mRNA from rat basophilic leukemia cells.

Immunoglobulin E-binding activity was expressed in Xenopus oocytes injected with mRNA from rat basophilic leukemia cells which possess abundant immunoglobulin E (IgE) receptor. Such activity was demonstrated with intact oocytes by their binding of 125I-labeled mouse monoclonal IgE. Binding activity was specific as shown by the total inhibition of 125I-IgE binding by unlabeled IgE but not by unlabeled IgG1. The relevance of the IgE-binding activity to the IgE receptor was also supported by the absence of this activity in oocytes injected with mRNA from cells lacking surface IgE receptors. mRNA coding for the IgE-binding activity was enriched in fractions sedimenting at 13.5 S in sucrose density gradients. From oocytes injected with rat basophilic leukemia mRNA, two major polypeptides were isolated by affinity purification on IgE immunoadsorbent. One (Mr = 31,000) is equivalent in size to the previously identified "receptor-associated protein;" the other (Mr = 40,000) is speculated to be a partially glycosylated or unglycosylated form of the alpha subunit of the IgE receptor. The binding of IgE-coated fluorescent microspheres by oocytes injected with rat basophilic leukemia mRNA demonstrated the surface expression of the IgE-binding proteins.

Animals↗

PubMed1984

IgE-mediated triggering signals for mediator release from human mast cells and basophils.

Human basophils were developed in suspension culture of mononuclear cells of cord blood in the presence of conditioned medium of phytohemagglutinin-stimulated human T cells, from which interleukin 2 had been eliminated. Approximately 50-90% of cells recovered after 2-4 wk of culture were basophil granulocytes, which bear receptors with high affinity for human IgE. Sensitization of the cells with human IgE followed by challenge with anti-IgE resulted in the release of histamine and arachidonic acid (AA). In both the cultured basophils and human lung mast cells, bridging of cell-bound IgE with anti-IgE induced a transient increase in phospholipid methylation and intracellular cyclic AMP (cAMP), and these processes were followed by Ca2+ uptake and release of both histamine and AA. As demonstrated in rat mast cells, evidence was obtained that the activation of a proteolytic enzyme and phospholipid methylation induced by the bridging of IgE receptors are involved in the subsequent increase in AMP, and are an essential step for transduction of triggering signals for mediator release.

Basophils↗

PubMedDate not supplied

[Human basophil degranulation in pollinosis: correlation with skin-test diameter (author's transl)].

A human basophil degranulation (HBD) performed on an enriched basophil suspension (by gradient density) was applied in 95 subjects with 3 dilutions of grass pollen extract. Concordance with intradermal skin-test (ST) results reached 90% for wheal and 94% for flare. In 45 positive ST subjects, mean (+/- s.e.m.) of degranulation index was 54,1 +/- 4,2, 54,9 +/- 4,7 and 35,7 +/- 4,9 respectively for dilutions of 10(-4), 10(-6) and 10(-8) of grass pollen. Mean was 6,1 +/- 1,6, 8,2 +/- 1,7 and 8,5 +/- 1,6 in 50 negative ST subjects. In positive ST patients, a significant correlation (r = 0,53 p less than 0,001) appeared between ST diameter (flare) and degranulation index. HBD appears as reliable as RAST or automated histamine analysis but more easy to perform. It permits pharmacological studies of drugs inhibiting human basophil degranulation.

Asthma↗

PubMed1983

Ultrastructure of the mouse blood basophil.

This work establishes the presence of basophils in mouse peripheral blood and describes their ultrastructure. In this species, the cytoplasmic granules, which are membrane-bound and relatively scarce, differ both in size and electron-density. The intragranular particle size is often markedly heterogeneous. All cytoplasmic organelles are visible including a well-defined Golgi and centriole. The bi-lobed or multi-lobed nucleus has peripherally condensed heterochromatin, nuclear pores and often nucleoli. The surface membrane is characteristically abundant in projections and associated cavities. The electron microscope image of the mouse basophil shows similarities to that of the human basophil, but appears different from that of the guinea pig, chicken and rat.

Animals↗

PubMed1977

The absence of a human thymus lymphocyte antigen (HTLA) on basophils and mast cells.

Basophilic granulocytes and mast cells of different species have been reported to originate from thymocytes and other lymphocytes. These observations were recently confirmed when evidence was given that thymic antigen is present on rabbit basophilic granulocytes. In the study reported here, human leukocytes were tested by the immunofluorescence technique and the immunoelectron-microscopy technique to ascertain whether a human thymus lymphocyte antigen (HTLA) could be detected on their surface. We could demonstrate the presence of HTLA on T lymphocytes but not on basophilic granulocytes, nor on mast cells in Cryostat sections of various tissues.

Antibodies↗