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PubMed2000

Functional consequences of FcepsilonRIalpha up-regulation by IgE in human basophils.

These studies examine the functional changes that occur after up-regulation of FcepsilonRIalpha by immunoglobulin E (IgE) for human basophils. Basophils were cultured with and without IgE antibody (PS myeloma IgE or anti-gp120-specific IgE) for 1 week and challenged with anti-IgE, anti-FcepsilonRIalpha, or antigen for histamine and IL-4 secretion. There were no statistically significant changes in their response to anti-IgE or anti-receptor antibodies, as compared with controls incubated for the same period, whereas receptor expression increased an average of 4-fold. There was increased responsiveness to antigenic challenge, most notably at suboptimal concentrations of antigen (gp120 peptide-ovalbumin conjugate). For a 6-fold difference in cell surface density of gp120-specific IgE, there was a 2.2-fold change in antigen potency or 3-fold increases in histamine release at lower antigen concentrations. Similar results were found for secretion of IL-4. Basophil sensitivity, which is a measure of the density of antigen-specific IgE required for 50% of maximal secretion, was used to determine whether up-regulation of FcepsilonRIalpha was coordinated with up-regulation of other components of the IgE-signaling pathway. The results indicated up-regulation of FcepsilonRI is not always accompanied by changes that allow sensitivity to be maintained. These results indicate that functional up-regulation does occur but that its magnitude may be modulated because not all components of the signaling pathway are up-regulated in a balanced manner.

Antibodies, Anti-Idiotypic↗

PubMed1965

Basophil degranulation induced by oral poison ivy antigen.

Seven subjects shown by patch test to be sensitive to poison ivy oleoresin were challenged with graded oral doses of ivy extract. In each instance the circulating basophil leukocytes showed significant degranulation within one hour of challenge. This finding was interpreted as evidence of the presence of immediate-type circulating antibody to ivy antigen in these subjects. No drop in the absolute basophil count was noted, but with higher oral doses the degranulation persisted for several days. Thirteen control subjects showed no change in the basophil morphology or count, indicating that the resin at these levels was not toxic to this cell. All but one of the sensitive subjects showed objective patch test evidence of hyposensitization following the intensive three-week course of oral poison ivy antigen.

Antigens↗

PubMed1976

Degranulation of basophilic leukocytes in allergic contact dermatitis reactions in man.

Basophilic leukocytes participating in allergic contact dermatitis in man underwent progressive degranulation over the course of several days after skin test. Less than 10% of basophils were degranulated in 24-hr reactions, but more than 60% were degranulated by 72hr. In electron microscopic individual basophil granules developed looser packing of particles by finely granular material, and eventual loss of all visible granule contents, changes that were progressive between 2- and 3-day reactions.

Adolescent↗

PubMed2003

[Chronic urticaria. Clinical evolution, autologous serum test, count and activation of basophils].

Recent advances on the pathogenesis of chronic urticaria have defined a group of patients with autoantibodies directed to the IgE or to the alpha chain of the Fc high affinity receptor of IgE, Fc epsilon RI alpha. These antibodies are detected in vivo through the autologous serum test (AST) and in vitro with a variety of techniques. We here describe 37 patients with chronic urticaria, 28 female and 9 male, with a f/m ratio of 3.1. Mean age at onset was 36.5 years (range 16-78). AST was positive in 25 (68%) of 37 patients. Serum induced a wheal significantly larger than plasma (122 +/- 78 mm2 vs 57 +/- 66 mm2, p < 0.05). Median persistence of the chronic urticaria, estimated by Kaplan-Meyer analysis, was 437 days, with no difference between AST(+) and AST(-) patients (437 vs. 369, p = 0.18). Mean IgE concentration was 157 +/- 173 IU/mL, as expected in an unselected population. Basophil count was lower in patients compared with controls (17 +/- 12 cel/microL vs. 43 +/- 27 cel/microL, p < 0.008). Only sera from 2/7 (28.6%) patients AST (+) and very low basophil count consistently induced expression of CD63. This effect was abrogated in non-releasing basophils, confirming the presence of antibodies directed to the Fc epsilon RI alpha-IgE. We conclude that functional antibodies are present in only a minority of patients and that their identification does not predict the outcome.

Adolescent↗

PubMed1992

[Reactivity of pulmonary mast cells and peripheral blood basophils in patients with sarcoidosis and bronchial asthma].

We have studied the sensitivity of pulmonary mast cells and blood basophils in patients with sarcoidosis and bronchial asthma. The cells were induced in vitro with anti-IgE. The histamine releasing from mast cells and basophils was high in both examined groups of patients. The histamine releasing from mast cells in patients with sarcoidosis was 27.8-47.1% and in asthmatic patients 42.8-58.9%. The histamine releasing from basophils was 38.2-57.9% and 41.0-62.1%, respectively. The high sensitivity of mast cells of patients with sarcoidosis may suggest that these cells play an essential role in pathology of this disease.

Adult↗

PubMedDate not supplied

[The characteristics of the action of ethanol in operators with different states of the skin tissue basophils].

The changes in some parameters of an operator activity after ethanol administration at a dose of 1.9 g/kg body weight in 10 men doing the job of two-dimensional compensatory tracking in simulator, have been studied. In this case, the population state of tissue basophils (mast cells) of the body by studying the amounts of various structural and metabolic forms of these cells, contained in the skin biopsies, was studied. The degree of deterioration in operator activity was evaluated separately for the subjects with the population characteristics of tissue basophils higher or lower than mean values. It is indicated that the subjects with a low initial number of tissue basophils exhibiting signs of a holocrine-typed secretion and with a more pronounced response of these cells to ethanol were characterized by a significantly higher degree of the impairing many parameters of operator activity. Such differences were especially marked immediately after ethanol administration and practically lacked 12 hours after.

Adult↗

PubMed1992

Regulation of human basophil activation. II. Histamine release is potentiated by K+ efflux and inhibited by Na+ influx.

Na+ and K+ are the major extra- and intracellular cations, respectively. We have thus studied the role of these ions on human basophil histamine release by modifying their transmembrane gradients or by increasing membrane ion fluxes using ionophores. 1) When external Na+ (reduced to 4 mM) was replaced by the nonpermeating Na+ substitute N-methyl-D-glucamine, the release of histamine was enhanced in 2 mM Ca2+ (from 37.5 +/- 8.0% in 140 mM Na+ to 68.5 +/- 9.1% in low Na+) and became possible in the presence of low Ca2+ (at 1 microM Ca2+: from 0.6 +/- 0.7% in 140 mM Na+ to 36.2 +/- 8.0% in low Na+); moreover, in low Na+, the release of histamine became partly independent on Ca2+ influx. 2) Increasing the Na+ influx with the cation channel-forming gramicidin D inhibited the release of histamine by 33.2 +/- 13.6% (n = 6) in an external Na(+)-dependent manner. 3) Decreasing K+ efflux using K+ channel blockers (4-aminopyridine, quinine, sparteine) inhibited histamine release in a dose-response manner. 4) The K+ ionophore valinomycin, which increases K+ efflux, slightly enhanced IgE-mediated histamine release when used alone, whereas it potentiated the release of histamine from leukocytes previously treated with 4-aminopyridine by 57.0 +/- 18.6% (n = 7). 5) Decreasing K+ efflux by increasing external K+ inhibited IgE-mediated release in a similar manner as Na+ did. The inhibitory effects of Na+ and high K+ were not additive, thus suggesting that both cations inhibited the release by a common mechanism. In conclusion 1) our data evidence that histamine release from human basophils is inhibited by Na+ influx and potentiated by K+ efflux; 2) they suggest that K+ channels are present on the basophil membrane and that Na+ and K+ fluxes act on histamine release most probably via modulation of membrane potential.

4-Aminopyridine↗

PubMed2004

[Effect of pranlukast on histamine release and leukotriene c4 (ltc4) generation from human peripheral basophils].

Human basophils may play a role in bronchial asthma. The effect of pranlukast on histamine release and LTC4 generation from human peripheral basophils was examined. Histamine release induced by FMLP and C5a was inhibited by pranlukast in concentration-dependent manner, whereas anti-IgE Ab-induced histamine release was not affected. Both anti-IgE Ab-and FMLP-induced LTC4 were inhibited by pranlukast. These results suggest that pranlukast may improve symptoms of bronchial asthma by inhibiting basophil function in addition to antagonizing Cys-LT receptor.

Basophils↗

PubMed1990

[Presence and functional role of an epitope of the second receptor for IgE (FcE RII) in mast cells and basophils in the rat].

Mast cells and basophils express the high affinity IgE receptor (FcERI) whereas the low affinity receptor for monomeric IgE (FcE RII) is present on macrophages, lymphocytes, eosinophils, platelets and Langerhans cells. Recent studies confirmed that the two receptors were totally distinct. The present work shows that a monoclonal antibody (BB10), able to bind to FcE RII on different cell populations, interacts with FcE RI expressing cells: rat peritoneal mast cells and a rat basophilic leukemia cell line (RBL 2 H 3). The structure recognized by BB10 is distinct from FcE RI and modulates the IgE-dependent histamine release. In conclusion, it appears that a common epitope with FcE RII is present on mast cells and basophils and that a functional relation might exist between this structure and FcE RI.

Animals↗

PubMedDate not supplied

[The effect of salbutamol on histamine release from basophils in vivo and in vitro].

In vivo and in vitro basophil histamine release inhibition by salbutamol was investigated in patients with bronchial asthma. The study involved 14 patients in stable period of the disease: FEV1 = 66-84% of the normal values. Histamine release was determined following an incubation of the isolated basophils with concanavalin A (Sigma Co., USA) or specific allergens (dust, grass pollens, mites; Bencard, UK). Histamine was assayed with isotope-enzymatic technique according to Shaff and Beaven with histamine N-methyltransferase. Salbutamol administered intravenously in the dose of 1 mg inhibited allergen-induced histamine release from the basophils isolated from patient's blood within 30 minutes. Salbutamol in the concentration of 8 X 10(-6) M inhibited in vitro histamine release induced by an allergen and concanavalin A.

Adult↗

PubMedDate not supplied

[Usefulness of testing histamine release from isolated human basophils in anti-allergic and anti-asthmatic drug assessment].

Histamine release from isolated human basophils test was used to evaluate an activity of: histamine receptors H1 and H2 blockers, agonists of beta-receptors, calcium channel blocking agents, hydrocortisone, and disodium cromoglycate (Intal). The study involved 84 patients hospitalized for the bronchial asthma. Basophils were isolated with Day's technique modified by Shov and Norn. Histamine was measured with Shov's spectrofluorimetric technique. It was found that histamine release from isolated human basophils may be used in both evaluation of the mechanism of action and efficiency of drugs used in allergic diseases therapy.

Asthma↗

PubMed1991

Low MW B-cell growth factor potentiates histamine release from human basophil leucocytes.

The aim of the present study was to evaluate the effects of a commercial preparation of low molecular weight (MW) B-cell growth factor (BCGF), a product of activated human T cells, on histamine release from stimulated human basophils. In all the 23 cases tested, BCGF enhanced significantly the histamine release from stimulated human basophil leucocytes. After leucocyte incubation with 1% v/v BCGF, anti-IgE-induced histamine release increased from 11.9 +/- 1.9% to 31.8 +/- 3.3% (mean +/- SEM; P less than 0.001), formyl-methionine peptide-induced histamine release increased from 24.9 +/- 3.9% to 50.3 +/- 5.3% (P less than 0.001) and complement-mediated (i.e. induced by zymosan-activated human serum) histamine release increased from 10.7 +/- 1.8% to 29.2 +/- 5.2% (P less than 0.001). The enhancing effect of BCGF on histamine release was related to dose, temperature and time, since it was optimal after incubation with 10% v/v BCGF at 37 degrees for 60 min. BCGF activity persisted when the cells were washed after incubation and could also be observed when leucocyte incubation was carried out in the absence of extracellular Ca2+. It is noteworthy that basophils which showed a low response to activating agents released significant amounts of histamine after incubation with BCGF. These observations support the hypothesis that lymphocytes and lymphocyte-derived products may play a role in triggering and maintaining allergic reactions.

Adult↗

PubMed1990

IL-3 promotes basophilic differentiation of KU812 cells through high affinity binding sites.

The myeloid precursor cell line KU812 exhibits a constitutive potential to differentiate into basophilic cells. In the present study, the influence of recombinant human (rh)IL-2, rhIL-3, and recombinant human granulocyte-macrophage-CSF on basophilic differentiation of KU812-F cells was studied. Of all cytokines tested, rhIL-3 induced a significant increase in formation of metachromatically granulated cells (from 10% in control cultures up to 30% in cultures supplemented with 100 U/ml of rhIL-3) as well as dose-dependent (1.5- to 3 fold) increase in cellular histamine in KU812-F cell cultures. In addition, KU812-F cells exposed to rhIL-3 bound more IgE antibody than cells cultured in control medium with up to 3.3-fold increases in the mean fluorescence intensity on days 2 and/or 5 compared with control (p less than 0.001). RhIL-3 failed to induce significant changes in expression of the Tac-reactive subunit of the IL-2R (CD25), surface aminopeptidase N (CD13), ICAM-1 Ag (CD54), or CD40 Ag on KU812-F cells. To investigate the mechanism of IL-3 action on KU812-F cells, receptor analyses were performed by using 125I-radiolabeled rhIL-3. Quantitative binding studies and Scatchard plot analyses revealed the presence of a single class of 1910 to 2460 high affinity IL-3-binding sites per KU812-F cell with an apparent dissociation constant of 1.22 to 2.35 x 10(-9) M. Together, these results show that rhIL-3 promotes basophilic differentiation of KU812-F cells through a specific receptor.

Antigens, CD↗

PubMed1978

An inherited anomaly of human eosinophils and basophils.

Inclusions staining gray or blue-gray in Romanowsky treated films were found in eosinophils and basophils in a family as an autosomal dominant anomaly without overt clinical effects. Associated with the inclusions were distinctive crystals which were different from the crystalloids of eosinophil granules and from Charcot-Leyden crystals. The restriction of the anomaly to eosinophils and basophils indicates that these are related more closely to each other than to neutrophils and mast cells, and suggests the existence of a separate stem cell for eosinophils and basophils.

Basophils↗

PubMed1990

[Blast crisis of chronic myelogenous leukemia with blasts expressing both immature B lymphocyte- and myelomonocyte-associated antigens and differentiating into basophils in vitro].

A 43-year-old woman with Ph1-positive chronic myelogenous leukemia (CML) was diagnosed as having blastic crisis. The phenotype of blasts was CD9+, CD10+, CD19+, CD11b+ and CD33+, suggesting the B Lymphoid and myeloid mixed lineage. Two color analysis of CD10 and CD33 revealed that 50% of blast cells had both B lymphocyte- and myelomonocyte-associated surface markers. Rearrangement of the immunoglobulin heavy chain gene was detected. After culturing blasts with 12-o-tetradecanoyl-phorbol 13 acetate (TPA), basophilic granules appeared in cytoplasm of the cells. These granules were positive for toluidine blue staining. This finding that the biphenotypic blasts expressing both B lymphoid and myelomonocytoid features differentiated into basophils suggests that blasts of this case are derived from a common progenitor of B lymphoid and myeloid lineages including basophil.

Adult↗

PubMed1985

Endogenous somatostatin-like peptides of rat basophilic leukemia cells.

The tetradecapeptide somatostatin (SOM 14) and a 28-amino acid biosynthetic precursor (SOM 28) are constituents of diverse neuroendocrine tissues that are released by noxious stimuli from a subset of sensory nerve endings, and substantially modify the functions of basophils and mast cells. SOM-like factors were detected initially in the fluid phase of suspensions of immunologically challenged rat basophilic leukemia cells (RBL), and were purified from ethanol/0.2 M acetic acid (3/1, v/v) extracts of replicate portions of 3 X 10(9) RBL. Sephadex G-25 columns resolved factors of over 10,000, 2000 to 4000, and 300 to 1200 daltons that are antigenically related to SOM 14, as assessed by a radioimmunoassay specific for SOM 14. Only the two larger factors were detected by a radioimmunoassay for SOM 28(1-14), which binds to prepro-SOM and SOM 28 but not SOM 14. Reverse-phase high performance liquid chromatography distinguished the two smaller SOM peptides of RBL from SOM 28 and SOM 14, respectively. Amino acid analyses showed major differences in composition between the 2000 to 4000 dalton SOM of RBL and SOM 28. Picomolar to nanomolar concentrations of both of the smaller SOM peptides of RBL inhibited the IgE-dependent release of histamine from basophils to the same extent as SOM 14. The finding of 3 to 5 ng of structurally unique SOM-like peptides per 10(8) RBL suggests that endogenous mechanisms analogous to those of specialized sensory neurons may regulate the expression of hypersensitivity.

Amino Acids↗

PubMed1985

Test of a theory relating to the cross-linking of IgE antibody on the surface of human basophils.

Recent mathematical models of bivalent hapten-induced histamine release from basophils predict that under appropriate conditions histamine release is maximum when cross-link formation is maximum, at a hapten concentration equal to 1/(2Ka), where Ka is the average affinity constant of the hapten for a single IgE binding site. To test this prediction we sensitized human basophils with a monoclonal anti-dinitrophenol IgE and generated histamine release dose-response curves with a bivalent hapten, alpha, epsilon-DNP-lysine. The monoclonal IgE has a published affinity constant of 7.1 X 10(7) M-1 for epsilon-DNP-lysine as determined by equilibrium dialysis. From the position of the maximum of the histamine dose-response curves, both in the presence and in the absence of monovalent DNP hapten, we determine that the sensitizing IgE has an intrinsic affinity constant of 6.9 +/- 0.5 X 10(7) M-1 for epsilon-DNP-lysine and 1.2 +/- 0.6 X 10(6) M-1 for alpha-DNP-lysine. The agreement between the two estimates of the epsilon-DNP-lysine affinity constant, one from histamine release experiments involving surface bound IgE and one from binding experiments involving IgE free in solution, 1) is consistent with a central prediction of the theory of cross-linking and 2) indicates that the hapten-binding properties of the IgE are unaffected by its being bound to Fc epsilon receptors on the basophil surface.

Basophils↗

PubMed1985

[Effect of pesticides on the release of histamine, chemotactic factors and leukotrienes from rat mast cells and human basophils].

The influence of pesticides on mediator release from rat peritoneal mast cells and human basophiles was studied. Mediators from mast cells and basophils are important factors in allergic and inflammatory reactions. Release of histamine from rat mast cells and human basophils is demonstrated by stimulation with dieldrin, DDT, heptachlor, heptachlorepoxid and biphenyl. This pesticide-induced histamine secretion is dose-dependent and requires Ca2+. In contrast, incubation with gamma-HCH, HCB and carbaryl produces no significant histamine release. Additive histamine secretion results from simultaneous stimulation of rat mast cells with pesticides and anaphylatoxin C5a. Further, secretion of eosinophil and neutrophil chemotactic factors from rat mast cells is induced during incubation with dieldrin, biphenyl and heptachlorepoxid. It is also demonstrated that pesticides can stimulate the generation of lipidmediators. Biphenyl, gamma-HCH, heptachlor, heptachlorepoxid, DDT and dieldrin cause the release of leukotriene C4 from rat mast cells. The possible role of these in vitro results is discussed.

Animals↗