Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BASOPHILS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed1990

Histidine decarboxylase in human basophilic leukemia (KU-812-F) cells. Characterization and induction by phorbol myristate acetate.

The human leukemic cell line KU-812-F is known to differentiate into mature basophil-like cells under serum-free culture conditions. In the present study, the activity of histidine decarboxylase (HDC), a histamine-forming enzyme, in KU-812-F cells was found to be high, ranging from 10 to 57 pmol/min/mg protein. The great variation in HDC activity appeared to be due to different percentages and degrees of maturity of basophil-like cells during differentiation of this cell line. The enzyme was inhibited by alpha-fluoromethylhistidine but not by carbidopa, was unable to form dopamine from L-3,4-dihydroxyphenylalanine, and had a Km value for histidine of 0.27 mM, indicating that it was HDC and not aromatic amino acid decarboxylase. The HDC activity increased 1.8-fold when the cells were stimulated by phorbol myristate acetate, which is known to activate protein kinase C, and this increase was blocked by staurosporine, a potent inhibitor of protein kinase C.

Alkaloids↗
PubMed1993

Inhibition of passive sensitization of human peripheral basophils by synthetic human immunoglobulin E peptide fragments.

To delineate the binding site in the human immunoglobulin E (IgE) molecule to the Fc epsilon receptor on basophils and mast cells, we chemically synthesized a total of 71 peptide fragments within the sequence Ser300-Lys547 in the human IgE molecule. The synthetic peptides were tested for their capacity to inhibit passive sensitization of human peripheral basophils with atopic patient's serum containing the specific IgE against dust mites in vitro. It was found that a peptide fragment, Pro345-Ile356, potently inhibited the passive sensitization. To clarify the minimal active core, various analogues, such as shortened, substituted (by Gly or Ala residue), omission and retro-sequence peptides, were synthesized and assayed. The results suggested that the sequence Pro345-Lys352 in the human IgE molecule would be an IgE binding site, and that a synthetic octapeptide, Pro345-Phe-Asp-Leu-Phe-Ile-Arg-Lys352, inhibited the passive sensitization, probably by occupying the Fc epsilon receptor sites on the cells.

Allergens↗
PubMed1994

A discrete mathematical model applied to human basophil activation.

In this paper we present a model for the histamine negative feedback on the human basophil degranulation and another one for the feed-forward of these basophils on the extra-cellular histamine. These two models allow us to suggest a characterisation of the incubation time.

Algorithms↗
PubMed1994

A non-linear compartmental model of human basophil activation.

In this paper human basophil activation is modelled by means of a system of differential equations. The resolution of this system allows the justification of the incubation period and the unwedging period existing between the human basophil degranulation and the liberation of histamine.

Algorithms↗
PubMed1981

Enrichment of human basophils.

A 3-step procedure is described in detail for producing 50% basophils in 50% yield from human blood. Leukocytes from dextran sedimented blood or preferably whole blood are sedimented on Hypaque-Ficoll, then on aqueous Hypaque, followed by adherence and elution from a column of glass beads. The cells appear normal and undergo specific histamine release after incubation with antigen. The procedure is relatively rapid and should allow further study of mechanisms of mediator release with more homogeneous populations of basophils. The first step also provides a 5 min separation of blood into a lymphocyte enriched mononuclear cell fraction and a granulocyte enriched fraction.

Basophils↗
PubMed1987

Standardization of basophil degranulation for pharmacological studies.

There is a need of a standard basophil degranulation test for diagnosis and for immunopharmacological studies. In order to obtain a sufficient concentration of basophils blood was sedimented at 1 g which gave a yield of 1500-3000 basophils/microliter instead of 50/microliter in whole blood. As the course of degranulation is exponential, it can be linearised using a logarithmic approximation Y = A0 + A1 log D where D is the allergen concentration. The application of this mathematical method permitted the collection of statistical information about the test itself. The coefficient of variation was less than 10%. The test can be used to compare the allergenic potency of different extracts of the same allergen.

Basophils↗
PubMed1989

Flow cytometric methods for the analysis of human basophil surface antigens and viability.

Fluorescence and flow microfluorometric methods have been established for the detection and evaluation of IgE-bearing human leukocytes in various cell preparations including those where basophils are present at low percentages. Quantitative techniques for the determination of basophil purity, viability, and cell surface antigens including IgE are described. Use of these methods will facilitate the identification and phenotypic analysis of human IgE-bearing cells in a wide variety of biological fluids.

Antigens, CD↗
PubMed1983

Inhibition of histamine release from human basophils in vitro by calmodulin antagonists.

Calmodulin is a ubiquitous and versatile Ca2+-binding protein that plays a pivoting role in cellular metabolism. We have investigated the possibility that calmodulin plays a role in immediate hypersensitivity reactions by evaluating the effects of two agents, trifluoperazine dihydrochloride (TFP) and the sulfonamide derivative N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) which selectively bind to calmodulin. TFP and W-7 cause a dose-dependent inhibition of histamine secretion from human basophils in vitro induced by several immunological (i.e., antigen and anti-IgE) and nonimmunological (i.e., formyl-methionine-containing peptide and the Ca2+ ionophore A23187) stimuli. These results indicating that two specific calmodulin antagonists are potent inhibitors of the secretory response of human basophils support the hypothesis that calmodulin may play a role in the control of the release of preformed mediators from human inflammatory cells.

Adult↗
PubMed1976

Cutaneous basophil hypersensitivity.

Cutaneous basophil hypersensitivity (CBH) is a distinct form of lymphocyte-mediated hypersensitivity in guinea pigs, separate both from classic delayed hypersensitivity (DH) and from the well-known antibody-mediated reactions. CBH, not DH, is the usual cellular immune response of this species to a wide variety of immunogens (e.g., allografts, certain parasites, and viruses) when these are presented in native form without supplementation with mycobacteria-containing adjuvants, thus attesting to the importance of this response in the guinea pig's overall immune defense mechanism. Basophil-containing, cell-mediated, delayed-onset reactions occur in other species, including man, as well.

Animals↗
PubMed1976

Mediator release from basophil granulocytes in chronic myelogenous leukemia.

Mediator release from the leukocytes of two patients with chronic myelogenous leukemia and basophilia was studied using rabbit antihuman IgE antibody. The release of histamine, slow reacting substance of anaphylaxis (SRS-A), platelet activating factor (PAF), chemotactic activity for neutrophils and eosinophils, and an inhibitor of eosinophil migration was observed. However, the release of SRS-A from the basophils of one patient and the release of chemotactic activity from both patients displayed unusual properties. During acceleration of the disease process, the basophils of one patient released maximal SRS-A activity at progressively lower concentrations of anti-IgE. Both patients released a high molecular weight factor (M.W. greater than 20,000) which enhanced the migration of neutrophils and eosinophils and a low molecular weight chemotactic factor (M.W. less than 500) which selectively attracted eosinophils. A double peak of eosinophil chemotactic activity was routinely observed for the low molecular weight factor; this was shown to represent the eosinophil chemotactic activity of histamine with relative inhibition of migration at the histamine peak. There was little release of the tetrapeptides, ECF-A, in these patients which facilitated demonstration of this eosinophilotactic activity of histamine. These results suggest that the eosinophil chemotactic activity observed in acute allergic reactions is the net effect of the release of multiple chemotactic factors.

Antibodies↗
PubMed1977

Detection of immediate hypersensitivity in rabbits by direct basophil degranulation.

The direct in vitro antigen-induced degranulation of rabbit basophils based on a simplified one-step method for the staining of these cells is reported. Degranulation was assessed by counting the number of basophils before and after exposure to antigen at 37 degrees C in the presence of Ca++. The degranulation was IgE-mediated, as shown by its passive transfer to nonimmunized rabbits by IgE-containing serum; also, the reaction was dependent on the presence of Ca++ ions and normal cell metabolism. The technique allowed the detection of serum factors capable of blocking the degranulation. It provided a means for following IgE sensitization at the cellular level, which is a better index of immediate hypersensitivity than the presence of circulating specific IgE.

Animals↗
PubMed1979

Cytotoxicity of ionophore A23187 for basophils and other human blood cells.

The calcium ionophore A23187(A23) at concentrations exceeding 1 microgram/ml has been shown to be progressively cytotoxic for human blood basophils, neutrophils, lymphocytes, and erythrocytes. Toxicity to basophils was considered to be manifested by the increasing inability of 2-deoxyglucose (2DG) to inhibit histamine release (HR) at increasing concentrations of A23. The toxicity to neutrophils and lymphocytes was demonstrated by decreased lactate production (LP) after incubation with A23 of Ficoll-Hypaque fractions greatly enriched in each respective cell type. Red cells present in dextran-sedimented leukocytes were increasingly susceptible to lysis during washing subsequent to exposure to increasing concentrations of A23. A concentration of 4 microgram A23/ml, which is cytotoxic at 37 degrees C, produced optimal and noncytotoxic HR at 22 degrees C. It was possible to reduce A23 concentrations required for optimal HR by increasing Ca++ from 0.6 to 3 mM.

Anti-Bacterial Agents↗
PubMed1982

Monoclonal antibodies to immunoglobulin G4 induce histamine release from human basophils in vitro.

Monoclonal murine antibodies to human IgE, IgG1, IgG2, IgG3, IgG4, IgM, and IgA1 were prepared and their abilities to stimulate histamine release from human peripheral blood leukocytes were investigated. As expected, anti-IgE caused 8% to 76% histamine release from the leukocytes of each of 14 nonallergic donors. In one subject anti-IgE alone had no effect, but a 15% histamine release did occur after the subsequent addition of a goat anti-mouse IgG antiserum to crosslink cell-bound anti-IgE molecules. Anti-IgG4 alone caused 5% to 59% histamine release from the cells of four of 14 donors. Subsequent challenge with goat anti-mouse IgG caused an additional release of up to 15% of the basophil histamine, but only from leukocytes of donors responsive to anti-IgG4 alone. No histamine release was detected after stimulation by monoclonal antibodies to IgG1, IgG2, IgG3, IgM, or IgA1. The results of this study indicate that monoclonal antibodies to IgG4 as well as to IgE can stimulate human peripheral blood leukocytes to release histamine. These observations support the theory that antigen-IgG4 interactions can stimulate histamine release from human basophils.

Animals↗
PubMed1984

In vitro basophil histamine release induced by mannitol in a patient with a mannitol-induced anaphylactoid reaction.

Anaphylactoid reactions in man are associated with the infusion of diagnostic and therapeutic agents. The etiology of such reactions remains unknown, but clinically they have the signs and symptoms that mimic those associated with in vivo histamine release. We report that the leukocytes of a patient who suffered an anaphylactoid reaction associated with the infusion of mannitol repeatedly released histamine in vitro when the leukocytes were challenged with low concentrations of mannitol (less than 0.1 M). In 44% deuterium oxide buffer, the patient's cells were tenfold more reactive to mannitol as compared to normal leukocytes and were pharmacologically modulated in a fashion similar to IgE-dependent release. The temperature optimum for this nonhyperosmolar (less than 0.1M) mannitol-induced, deuterium oxide-dependent release was the same as that for IgE-dependent release. Desensitization of the patient's cells with anti-IgE completely suppressed release induced by low concentrations of mannitol but did not affect the hyperosmolar (greater than 0.1M) mannitol-induced release of basophil histamine. These studies suggest that patients experiencing anaphylactoid reactions may be identified by use of in vitro basophil histamine release.

Anaphylaxis↗
PubMed1988

Recombinant human interleukin-1 beta causes histamine release from human basophils.

Histamine releasing factors (HRFs) have been demonstrated to be secreted by human lymphocytes and monocytes (alveolar macrophages); however, none has been purified to date. Because of the similarity of our HRF to the physical chemical properties of interleukin-1 (IL-1) and tumor necrosis factor (TNF), we have assessed the ability of preparations of IL-1 and TNF to cause basophil histamine release (HR). Human recombinant pro-IL-1 beta, recombinant mature IL-1, and, to a lesser extent, human recombinant TNF caused significant HR from a subpopulation of donor basophils. The pro-IL-1 beta elicited a dose response between 40 and 800 ng/ml; higher concentrations were inhibitory. Approximately 30% of subjects tested are responsive to either mature IL-1 or TNF. These share the same responder subset, but the magnitude of the TNF response is considerably less. A response to the pro-IL-1 was restricted to those subjects with prominent HR to anti-IgE; the response to mature IL-1 and TNF was unrelated to the response to anti-IgE. As in other functional assays, the pro-IL-1 is 50- to 100-fold less potent than mature IL-1, and unlike human HRF, it is highly unstable and rapidly loses activity. Mononuclear cell-derived HRF differs in physicochemical properties from IL-1 or TNF; nevertheless, it appears likely that a variety of cytokines may possess histamine-releasing capability.

Antibodies, Anti-Idiotypic↗
PubMed1992

Connective tissue-activating peptide-III and its derivative, neutrophil-activating peptide-2, release histamine from human basophils.

Connective tissue-activating peptide-III (CTAP-III) is a 9 kd platelet alpha-granule-derived growth factor. It stimulates the synthesis of DNA, hyaluronic acid, glycosaminoglycans, and proteoglycan core protein in human fibroblasts. Human mononuclear cell-derived proteases have been previously demonstrated to digest the N-terminal 15 residues of CTAP-III (total, 85 residues) to produce neutrophil-activating peptide-2 (NAP-2). CTAP-III and NAP-2 belong to a class of proteins (platelet factor 4, interleukin-8/NAP-1, etc.) associated with inflammation and wound repair. In our efforts to purify human mononuclear cells and platelet-derived histamine-releasing factors, we had previously discovered that mixtures of CTAP-III and NAP-2 released histamine from human basophils. We have now developed simple protocols for the purification of CTAP-III and NAP-2, independently, from calcium ionophore (A23187)-stimulated platelet supernatants by affinity chromatography and have established their identity by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and N-terminal sequence analysis. Each of these related histamine between 2 and 10 micrograms/ml, a range identical to that obtained with CTAP-III/NAP-2 mixtures that we reported earlier. Thus, our data suggest that CTAP-III and NAP-2 independently release histamine from human basophils in dose ranges similar to ranges required for fibroblast stimulation by each.

Basophils↗
PubMed1987

The effect of co-operativity on the equilibrium binding of symmetric bivalent ligands to antibodies: theoretical results with application to histamine release from basophils.

A theory for the co-operative binding of bivalent ligands to cell surface or solution antibody is presented. The theory treats both negative co-operativity, where the binding of a ligand to one site on an antibody makes it more difficult to bind to the second site, and positive co-operativity, where the binding of a ligand to one site on an antibody makes it easier to bind to the second site. Candidates for bivalent ligands exhibiting negative co-operativity (caused probably by steric hindrance) are certain anti-immunoglobulin antibodies. We show how to calculate the amount of ligand bound, the fraction of antibody in cross-links (i.e. in ligand-antibody aggregates) and the fraction of antibody in any size ligand-antibody aggregate. With sample calculations it is demonstrated that there can be major differences in the binding and cross-linking properties of co-operative and non-co-operative bivalent ligands. We discuss how the theory can be used to analyze experiments where human basophils or rat basophilic leukemia cells are exposed to bivalent ligands that bind co-operatively to immunoglobulin E.

Animals↗
PubMed1995

An abnormal clone with monosomy 7 and trisomy 21 in the bone marrow of a child with congenital agranulocytosis (Kostmann disease) treated with granulocyte colony-stimulating factor. Evolution towards myelodysplastic syndrome and acute basophilic leukemia.

Cytogenetic analysis of bone marrow cells revealed an abnormal clone with monosomy 7 and trisomy 21 in a 12-year-old child with Kostmann disease (KD). The patient presented with anemia, thrombocytopenia, and splenomegaly after 5 years of treatment with granulocyte colony-stimulating factor (G-CSF). The bone marrow morphology was consistent with the diagnosis of myelodysplastic syndrome (MDS). Administration of G-CSF was discontinued at this point. Bone marrow studies 2 and 5 months later showed persistence of both myelodysplasia and the abnormal clone with monosomy 7 and trisomy 21. Monosomy 7 was also confirmed by fluorescence in situ hybridization (FISH). After 2 months of follow-up, the patient presented with acute basophilic leukemia, a very rare variant of acute myeloid leukemia (AML), expressing the same bone marrow chromosome abnormalities as observed earlier. This is a rare case of KD with prolonged survival and a cytogenetically abnormal clone evolving to MDS and acute basophilic leukemia. The significance of monosomy 7 and trisomy 21 in KD treated with G-CSF is discussed.

Agranulocytosis↗