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PubMed1987

Rapid phosphorylation of a 92,000 MW protein on activation of rat basophilic leukaemia cells for histamine release.

Many cellular functions are modulated by phosphorylation of proteins. The IgE- or ionophore-mediated activation of rat basophilic leukaemia cells (RBL-2H3) was accompanied by the prominent phosphorylation of a 92,000 molecular weight (MW) cellular component. The degree of phosphorylation of this component correlated with the extent of histamine release from the cells. This phosphorylation was rapid, reaching a maximum 2-5 min following the addition of the ionophore or antigen, and decreasing to background by 30 min. In contrast, histamine release is a much slower process. Although the phosphorylation required the presence of Ca2+ in the medium, it was not inhibited by La3+, which blocks the stimulated entry of Ca2+. Therefore, the stimulation of a Ca2+-dependent kinase is an early event in the activation of the rat basophilic leukaemia cells.

Animals↗
PubMed1987

Effects of ADP-ribosylation of GTP-binding protein by pertussis toxin on immunoglobulin E-dependent and -independent histamine release from mast cells and basophils.

Pretreatment of rat peritoneal mast cells, human basophils, bone marrow-derived mouse mast cells (BMMC) and mouse mast cell line PT-18 cells with 1 microgram/ml pertussis toxin (PT) failed to inhibit immunoglobulin E (IgE)-dependent histamine release from the cells. In BMMC and PT-18 cells, even 20-hr incubation of the cells with 1 microgram/ml PT, which ADP-ribosylates more than 97% of 41 kDa, alpha-subunit of Ni in the cells, failed to affect the IgE-dependent release of histamine or arachidonate. The results indicate that GTP-binding protein, Ni, is not involved in the transduction of triggering signals induced by cross-linking of IgE receptors. In contrast, pretreatment of rat mast cells with 1 ng/ml to 0.1 microgram/ml PT for 2 hr inhibited histamine release induced by compound 48/80 in a dose-dependent manner. A similar pretreatment with PT inhibited thrombin-induced histamine release from BMMC and N-formyl-L-methionyl-L-leucyl-L-phenylalanine-induced histamine release from human basophils in a similar dose-dependent fashion. However, even 20 hr of incubation of sensitized BMMC with 1 microgram/ml PT failed to inhibit either thrombin-induced or antigen-induced breakdown of phosphatidylinositides (PI), i.e., the formation of inositol triphosphate and diacylglycerol, Quin-2 signal, and the release of arachidonic acid. The results indicate that the inhibition of thrombin-induced histamine release by PT-treatment is not due to the inhibition of PI-turnover, and that Ni is not involved in thrombin-induced or antigen-induced (IgE-dependent) hydrolysis of phosphatidylinositides in mast cells.

Adenosine Diphosphate Ribose↗
PubMedDate not supplied

Does basophil releasability contribute to bronchial hyperreactivity in asthma?

Histamine inhalation test and basophil degranulation test in polymxin B were performed in 21 atopic asthmatic patients. Basophil degranulation in vitro was observed in 11 patients. Positive results of the degranulation test occurred with simular frequency in patients with high and low PC20. No significant correlation between PC20 and the magnitude of degranulation was found (r = 0.09).

Asthma↗
PubMed1987

Comparison of the effects of clonidine and guanfacine on the histamine liberation from human mast cells and basophils and on the human bronchial smooth muscle activity.

The inhibitory effects of clonidine and guanfacine on antigen-induced histamine release from human basophils and mast cells and on bronchial muscle tension were compared. Clonidine, but not guanfacine inhibited the antigen-induced histamine release from human basophils and mast cell preparations. This effect of clonidine was prevented by an H2-antagonist, cimetidine. Clonidine and guanfacine, like norepinephrine, inhibited the twitch contraction of electrically stimulated human segmental bronchi by stimulation of alpha 2-adrenoceptors. Clonidine and guanfacine had no effects on the basal bronchial muscle tone, but in very high concentrations they could reduce a carbacholine-induced bronchial tone. It is suggested that the inhibitory effects of clonidine on allergic reactions and on exicitatory nerve transmission in human airways may be useful in the treatment of asthmatic patients.

Adrenergic alpha-Agonists↗
PubMed1987

Phototoxicity of non-steroidal anti-inflammatory drugs demonstrated in vitro by a photo-basophil-histamine-release test.

The phototoxic activity of the non-steroidal anti-inflammatory drugs (NSAID) acetylsalicylic acid, benoxaprofen, carprofen, diclofenac, indoprofen, ketoprofen, tiaprofenic acid, and of thiophene, a heterocyclic ring structure of the tiaprofenic acid molecule, was evaluated in vitro by a newly developed photo-basophil-histamine-release test (PBHRT) performed with human leukocytes. Cell suspensions incubated with 10(-6) to 10(-3) M of the test compounds were exposed to 1 to 100 J/cm2 UVA. Maximum photo-basophil-histamine-release was 4% with acetylsalicylic acid, 10% with benoxaprofen, 20% with thiophene, 28% with diclofenac, 39% with tiaprofenic acid, 40% with carprofen, 55% with ketoprofen, and not demonstrable with indoprofen. These results indicate that many NSAID can exert phototoxic effects, thus confirming clinical observations as well as other in vitro experiments. The PBHRT seems to be a promising new method for the identification of phototoxic compounds.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

[Basophil degranulation test in suspected mould allergy].

Mould allergy is often linked with a pattern of signs and symptoms of the upper airways, especially of the nose. Since exact aetiopathological correlations are hard to determine by anamnesis only, further allergy diagnosis is very important. This often yields marked differences between intracutaneous and nasal provocation tests. The human basophil degranulation test (HBDT) now offers a further method of in-vitro diagnosis. This test can explore the condition of the basophils, which are of great importance for the allergic reaction besides the mast cells, and the ability of these cells to degranulate in the presence of a corresponding allergen. We investigated the correlations between the results of HBDT, intracutaneous skin test and nasal provocation test. 30 patients with perennial rhinitis suspected of being caused by moulds were tested using 4 mould mixtures. We found many more positive results with the nasal test and HBDT than with the skin test. The corrected contingency coefficient after Pearson showed a stronger correlation of HBDT to the incracutaneous skin test and to the nasal provocation test than between the two in-vivo methods. This is thought to be due to a wider sensitivity spectrum of the degranulation test which can possibly also measure other allergy reactions than type I after Commbs and Gell. We consider HBDT to be a valuable additional tool in allergy diagnosis. We should welcome a wider range of different allergenic test slides and a standardisation of allergenic extracts.

Adolescent↗
PubMed1988

Demonstration of idiotypes expressed on basophil-bound IgE antibodies by using anti-idiotype-induced histamine release in grass pollen-allergic patients.

This study was designed to analyse further the idiotypic cross-reactivity between anti-Lol p I murine monoclonal antibodies of IgG isotype and basophil-bound human IgE antibodies from grass pollen-sensitive patients. It was also designed to determine the expression frequency of the idiotypes present on cell-bound IgE. Rabbit anti-idiotypic antisera were produced against idiotypes of three anti-Lol p I monoclonal antibodies (290A-167, 539A-6 and 348A-6) of different specificities. Basophils from 19 patients reacting to Lol p I allergen, as shown by positive skin test reactions and by the presence of serum-specific IgE antibodies (measured by RAST), were challenged with these rabbit anti-idiotypic antibodies and the histamine released was measured. Our data indicate that IgE-borne idiotypes were expressed as follows: (i) co-expression of the three idiotypes in 15% of patients; (ii) co-expression of two idiotypes in 21% of patients; and (iii) expression of a unique idiotype (290A-167) in 42% of patients. Among the three idiotypes, 290A-167 was shown to be a public idiotype since it was expressed in 80% of patients. Fab fragments of anti-idiotypic antibodies could inhibit anti-idiotype-induced histamine release, but optimal conditions varied from one patient to another.

Adult↗
PubMedDate not supplied

A comparative study of the RAST, indirect haemagglutination, basophil degranulation and latex tests in the diagnosis of human hydatid disease.

In order to compare the diagnostic efficacy of the, basophil degranulation, RAST, indirect haemagglutination and latex tests, we carried out these four tests on 50 patients with confirmed hydatid disease due to Echinococcus granulosus. As a control group we employed 50 subjects who showed no evidence of hydatid disease or any other parasitic disease. The test which displayed the highest degree of diagnostic efficacy was the basophil degranulation test with a sensitivity of 93% and an accuracy of 97%. Next in diagnostic efficacy were the haemagglutination and RAST tests with very similar results-a sensitivity of 82% and an accuracy of 91% for the former, and for the latter a sensitivity of 80% and an accuracy of 90%. The latex test, with a sensitivity of 67% and an accuracy of 83%, possessed the lowest degree of diagnostic efficacy. There is an obvious decrease in the sensitivity of the tests when the localization of the cyst exclusively pulmonary; in these cases the RAST test was positive in only 50%, and the degranulation test in 77.7%.

Adolescent↗
PubMed1988

Histamine release from human basophils by synthetic block co-polymers composed of polyoxyethylene and polyoxypropylene and synergy with immunologic and non-immunologic stimuli.

Co-polymers composed of polyoxyethylene and polyoxypropylene have been shown previously to trigger histamine release from mouse peritoneal mast cells; this property quantitatively is directly related to the ionophorous ability of these compounds to cause a functional exchange of intracellular K+ for extracellular Na+ across the cell membrane. We investigated the effect of an inflammatory copolymer, T130R2, on human basophils. The data demonstrate that T130R2 can cause calcium-dependent histamine release from human basophils in vitro. Further, at concentrations that do not cause histamine release, this co-polymer markedly augments release by suboptimal concentrations of the lectin Con A or anti-IgE antibody and the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate but not the calcium ionophore A23187. Thus, these co-polymers induce mediator release from cells of both rodents and humans. In both instances it is likely that calcium-dependent cell triggering is the result of an influx of sodium ions with concomitant depolarization of the transmembrane potential. In common with the calcium ionophore A23187, the co-polymer T130R2 has the ability to synergize with stimuli which trigger the IgE receptor as well as those which directly activate the cellular calcium- and phospholipid-dependent protein kinase.

Adjuvants, Immunologic↗
PubMed1989

Protein kinase C (PKC) changes in human basophils. IgE-mediated activation is accompanied by an increase in total PKC activity.

We have examined the changes in protein kinase C (PKC) which follow IgE-mediated activation of basophils. Exposure to 0.1 microgram/ml anti-IgE resulted in an increase in total cellular PKC (169 +/- 23% of control, histamine release (HR) = 33 +/- 7%, n = 12) which could be accounted for solely by the increase in membrane-associated PKC. These changes reached a maximum (280 +/- 48%) 1.0 min after challenge and declined to 190 +/- 38% after 5.0 min though histamine release was not complete until 5 to 10 min later. We found a good correlation between the increase in membrane-associated PKC and the eventual release of histamine (rs = 0.902). Donors whose basophils released less than 5% total histamine (n = 3, HR = 3 +/- 1%) showed a partial activation of PKC (173 +/- 18%) though much less than the remaining donors (increase in PKC = 346 +/- 59%, n = 9, HR = 43 +/- 7%). We observed no redistribution of cytosolic PKC at any time following exposure to anti-IgE. In contrast, 0.1 microgram/ml 2-O-tetradecanoyl-phorbol-13-acetate (HR = 36 +/- 3%, n = 3) promoted an increase in total cellular PKC, the loss of 31 +/- 4% of the cytosolic PKC and an 816 +/- 183% increase in membrane-associated PKC. Activation of PKC by anti-IgE was only partially dependent on extracellular calcium. In the absence of calcium, the increase in PKC was approximately 65% (n = 4) of that noted in the presence of 1mM calcium but these levels were sustained over much longer periods, failing to return to base line after 30 min. Higher than normal concentrations of calcium (5 to 10 mM) promoted rapid increases in PKC activity and accelerated the return to base line (back to prechallenge levels by 5 min). Suboptimal concentrations of anti-IgE (0.01 microgram/ml) attenuated the changes in membrane associated PKC and altered the kinetics of the response. The time required to reach maximum activity increased from 1.0 to 5.0 min with a corresponding decrease in the rate at which histamine was released. Higher concentrations of anti-IgE (1.0 microgram/ml) promoted a rapid increase in PKC (maximum increase in PKC = 501 +/- 59%, time = 0.5 min, HR = 28 +/- 2%) followed by an equally rapid return to base line levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Basophils↗
PubMed1989

Pharmacological control of human basophil histamine release stimulated by eosinophil granule major basic protein.

Eosinophil granule major basic protein (MBP) is a 13,800 MW arginine-rich polypeptide that is unique among basic molecules in its ability to stimulate human basophil histamine release. We examined the Ca2+ requirements and pharmacological regulation of MBP-stimulated histamine release. Minimal MBP-induced histamine release occurred in the absence of extracellular Ca2+, whereas addition of 0.1 mM Ca2+ resulted in 70% of the maximum histamine release response. Maximum histamine release required 0.5 to 1 mM extracellular Ca2+. The MBP-induced histamine release was blocked by a calmodulin antagonist and by theophylline and was partially inhibited by an inhibitor of phospholipase A2. Release was unaffected by inhibition of protein kinase C. Basophil pretreatment with pertussis toxin also resulted in a concentration-dependent inhibition of release, suggesting involvement of a GTP regulatory protein in the activation mechanism. Histamine release stimulated by a 13,900 MW poly-L-arginine exhibited a dissimilar pharmacological profile from that of MBP. These results support the non-cytolytic nature of the MBP activation mechanism and identify pharmacological approaches for control of MBP-induced mediator release.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Effects of human recombinant interleukin 5 and 3 on the differentiation of cord blood-derived eosinophils and basophils.

When mononuclear cells from umbilical-cord blood were cultured for 3 weeks, low concentrations of interleukin 3 supported the preferential growth of basophils, with eosinophils comprising a smaller proportion. These basophils contained 0.15-0.3 microgram histamine per 10(6) cells, and released histamine by the IgE-dependent and -independent stimuli. Interleukin 5 increased the number and proportion of eosinophils in a dose-dependent manner without affecting the proliferation of other cell types in the interleukin 3-supplemented cultures. These cultured eosinophils could be activated by platelet-activating factor.

Basophils↗
PubMed1989

[Functiono-morphologic characteristics of tissue basophils of the human skin based on electron microscopic data].

A study is presented of the ultrastructure of tissue basophils evaluated by electron microscopy in patients with rheumatism and rheumatoid arthritis. Four types of cells were distinguished according to their functional activity and morphological manifestations. Qualitative analysis of the population of tissue basophils allows to establish a relationship with such characteristics of the clinical picture as activity of the inflammatory process primarily and to analyze in detail the role and significance of these cell forms in the process of formation of inflammatory changes in the connective tissue.

Arthritis, Rheumatoid↗
PubMed1985

[Circulating and basophil-fixed specific IgE in human alveolar echinococcosis].

Biological parameters of immediate type hypersensitivity were assessed in 19 patients with alveolar echinococcosis. Serum total IgE concentrations were higher than normal values in 12 patients, and parasite-specific IgE were present in 9 patients. A significant relationship was observed between these two parameters. Evolution of specific IgE during a 1-year period appeared to correlate with surgical removal of parasitic material; it did not correlate with the clinical evolution in patients treated with mebendazole. Specific basophil fixed-IgE were demonstrated using both a basophil degranulation test and a histamine release test in the 19 patients under study, including serologically negative and circulating specific IgE-negative patients.

Basophils↗
PubMed1988

A monoclonal antibody that inhibits secretion from rat basophilic leukemia cells and binds to a novel membrane component.

Rat basophilic leukemia (RBL-2H3) cells, like mast cells and basophils, carry monovalent membrane receptors with high affinity for IgE (Fc epsilon R). Cross-linking of these receptors provides the immunologic stimulus which initiates a series of biochemical events, culminating in secretion of inflammatory mediators. In an attempt to identify membrane components involved in the stimulus-secretion coupling of these cells, hybridomas were produced from splenocytes of mice immunized with intact RBL-2H3 cells. Here we report the production of a mAb (designated G63) that inhibits the Fc epsilon R-mediated secretion from RBL cells. At low degrees of Fc epsilon R aggregation, the mAb G63-induced inhibition may be complete, whereas at the maximum of secretion the inhibition is in the range of 30 to 40%. The relative degree of inhibition of secretion is dependent on the dose of mAb G63. Furthermore, inhibition requires the bivalency of G63, as the Fab fragments are inactive. The number of antigenic epitopes recognized by G63 per RBL-2H3 cell is 1.8 x 10(4) epitopes/cell, as determined by direct binding studies of 125I-labeled Fab fragments of G63. This number is 20 to 30 times smaller than that of Fc epsilon R on the same cells. The membrane component to which G63 binds has been identified by immunoprecipitation as a glycoprotein with an apparent Mr of 58 to 70 kDa. All of these results, and the fact that no competition for binding to RBL cells between mAb G63 and IgE can be resolved, indicate that mAb G63 binds to a membrane component which is distinct from the Fc epsilon R. mAb G63 suppresses the Fc epsilon R-mediated rise in cytoplasmic concentration of free Ca2+ ions, known to be one of the biochemical signals involved in the stimulus-secretion coupling in RBL-2H3 cells. G63 does not affect, however, the degranulation induced by the Ca2+ ionophore A23187. Therefore, mAb G63 probably exerts its inhibitory effect on a step preceding the rise in cytoplasmic free Ca2+. Thus, mAb G63 defines a previously unidentified membrane component that is involved in one of the early steps of the RBL-2H3 activation mediated by their Fc epsilon R.

Animals↗
PubMed1988

Whole body X-irradiation and repopulation with syngeneic bone marrow have no significant effect on basophils and mast cell compartment of murine lymph nodes.

In mice the atrophy of lymph nodes following a whole body X-irradiation with a dose of 800 R is not followed by a depletion of their basophils and mast cells content. Repopulation of irradiated mice with syngeneic bone marrow cells has no significant effect on the basophils and mast cells number in the popliteal lymph nodes.

Animals↗
PubMed1988

Basophils exhibit rearrangement of the bcr gene in Philadelphia chromosome-positive chronic myeloid leukemia.

Basophils were isolated from the peripheral blood of two patients with Philadelphia positive-chronic myeloid leukemia using monoclonal antibody Bsp-1 and fluorescence activated cell sorting. DNA blot analyses demonstrated rearrangement of the breakpoint cluster region gene in the isolated basophils, which suggests their leukemic origin. Isolated T cells from these patients that were cultured for 14 days in the presence of interleukin-2 lacked rearrangement of the breakpoint cluster region gene and are therefore unlikely to be derived from the chronic myeloid leukemia clone.

Basophils↗
PubMed1987

Anti-T cell monoclonal antibodies in vivo. I. Inhibition of delayed hypersensitivity but not cutaneous basophil hypersensitivity reactions.

As part of a study of the therapeutic potential of anti-T cell monoclonal antibodies, we studied the biologic effects of 8BE6, a mouse anti-guinea pig (GP) pan-T cell monoclonal antibody, on blood and tissue T cells and on the prototypic T cell-mediated reactions, classic delayed hypersensitivity (DH) and cutaneous basophil hypersensitivity (CBH). 8BE6 reacts to a 68,000 m.w. protein probably homologous with human CD5 (T1) and murine Lyt-1. A single dose of 1.8 to 3.4 mg 8BE6 caused lymphopenia and greater than 90% depletion of 8BE6+ peripheral T cells 1 to 72 hr later, and a significant but lesser decrease of lymphocytes reacting with another pan-T cell monoclonal antibody (p less than 0.02 at 24 hr). Free serum 8BE6 was detected for up to 48 hr after administration. Immunoperoxidase stains of tissue revealed that lymphocytes in lymph nodes and spleen were coated with mouse immunoglobulin 1 hr after antibody treatment and displayed in situ capping. Subsequently, there was a loss of T cells in all tissues (spleen, lymph node, liver, and kidney) except the thymus, with normal 8BE6 antigen staining returning by 72 hr. Areas of induration of DH reactions to PPD were reduced in 8BE6-treated GP, compared with pretreatment reactions in the same GP or in control-treated GP (p less than 0.001 for both). The numbers of infiltrating T cells and fibronectin-receptor-positive macrophages were also reduced. In contrast, 8BE6 had no effect on CBH reactions, as judged by erythema and basophil counts in 1-micron sections, although fewer T cells were found in reaction sites. There were no differences in IgM, fibronectin, or Ia staining between 8BE6-treated GP and controls. In vivo administration of a single dose of anti-T cell monoclonal antibody results in a transient, highly specific depletion of T cell populations in peripheral blood and tissues except the thymus. This treatment inhibits DH but not CBH reactions by systemic and local depletion of T cells.

Animals↗