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At least 1,351 records · Page 75Linked to original sources
PubMed1973

Surface IgE on human basophils during histamine release.

The distribution of surface IgE on human basophils was studied using fluorescence microscopy and immunoferritin electronmicroscopy. Redistribution of the IgE was dose, time and temperature dependent and required divalent anti-IgE. Cells which can release histamine in vitro were indistinguishable in these respects from cells which cannot. The redistribution was unaffected by the presence or absence of Ca(++). No correlation between the conditions required for optimal histamine release and for redistribution was observed. At low doses, optimal histamine release occurred in the absence of, or before, redistribution. At higher doses redistribution occurred in the absence of histamine release. Antigen-induced histamine release was unaccompanied by gross redistribution of the surface IgE. Since both histamine release and redistribution require bridging of IgE on basophils it is concluded that only certain kinds of cross-linking of the IgE effectively stimulates these cells.

Animals↗
PubMed1983

Activation of basophil and mast cell histamine release by eosinophil granule major basic protein.

Major basic protein (MBP) is a primary constituent of eosinophil granules. In this report, we demonstrate that MBP from human eosinophil granules initiates a nonlytic histamine release from human leukocytes. A direct effect of MBP on basophils was confirmed using purified human basophils. The kinetics of release were similar to those reported for poly-L-arginine, although MBP was less potent than poly-L-arginine of similar molecular weight. Reduction and alkylation of MBP diminished both the potency and efficacy of the molecule. Native MBP also stimulated histamine secretion from purified rat peritoneal mast cells in a manner characteristic of other polycations. These results emphasize the bidirectional nature of the basophil/mast cell-eosinophil regulatory axis.

Animals↗
PubMed1996

An immunoglobulin E-dependent recombinant histamine-releasing factor induces interleukin-4 secretion from human basophils.

A novel recombinant histamine-releasing factor (rHFR), which stimulates secretion from a subpopulation of human basophils that express a particular type of immunoglobulin E (IgE) or IgE+, was found to induce interleukin-4 (IL-4) production from cells isolated from these same donors. The secretion of IL-4 protein induced by rHRF significantly correlated with histamine release and the amount of protein generated, and the kinetics were identical to those caused by anti-IgE activation. Furthermore, the ability of rHRF to induce IL-4 protein production from cells not normally responsive to this protein was transferred by passive sensitization with plasma containing IgE+ antibody. That this novel protein stimulates both mediator release and the secretion of IL-4 protein from human basophils suggests a prominent role for this molecule in allergic disease.

Basophils↗
PubMed1997

Eotaxin-2, a novel CC chemokine that is selective for the chemokine receptor CCR3, and acts like eotaxin on human eosinophil and basophil leukocytes.

A novel human CC chemokine consisting of 78 amino acids and having a molecular mass of 8,778.3 daltons (VVIPSPCCMF FVSKRIPENR VVSYQLSSRS TCLKAGVIFT TKKGQQ SCGD PKQEWVQRYM KNLDAKQKKA SPRARAVA) was isolated together with three minor COOH-terminally truncated variants with 73, 75, and 76 residues. The new chemokine was termed eotaxin-2 because it is functionally very similar to eotaxin. In terms of structure, however, eotaxin and eotaxin-2 are rather distant, they share only 39% identical amino acids and differ almost completely in the NH2-terminal region. Eotaxin-2 induced chemotaxis of eosinophils as well as basophils, with a typically bimodal concentration dependence, and the release of histamine and leukotriene C4 from basophils that had been primed with IL-3. In all assays, eotaxin-2 had the same efficacy as eotaxin, but was somewhat less potent. The migration and the release responses were abrogated in the presence of a monoclonal antibody that selectively blocks the eotaxin receptor, CCR3, indicating that eotaxin-2, like eotaxin, acts exclusively via CCR3. Receptor usage was also studied in desensitization experiments by measuring [Ca2+]i changes in eosinophils. Complete cross-desensitization was observed between eotaxin-2, eotaxin and MCP-4 confirming activation via CCR3. No Ca2+ mobilization was obtained in neutrophils, monocytes and lymphocytes, in agreement with the lack of chemotactic responsiveness. Intradermal injection of eotaxin-2 in a rhesus monkey (100 or 1,000 pmol per site) induced a marked local infiltration of eosinophils, which was most pronounced in the vicinity of postcapillary venules and was comparable to the effect of eotaxin.

Amino Acid Sequence↗
PubMed2001

Prostaglandin D2 selectively induces chemotaxis in T helper type 2 cells, eosinophils, and basophils via seven-transmembrane receptor CRTH2.

Prostaglandin (PG)D2, which has long been implicated in allergic diseases, is currently considered to elicit its biological actions through the DP receptor (DP). Involvement of DP in the formation of allergic asthma was recently demonstrated with DP-deficient mice. However, proinflammatory functions of PGD2 cannot be explained by DP alone. We show here that a seven-transmembrane receptor, CRTH2, which is preferentially expressed in T helper type 2 (Th2) cells, eosinophils, and basophils in humans, serves as the novel receptor for PGD2. In response to PGD2, CRTH2 induces intracellular Ca2+mobilization and chemotaxis in Th2 cells in a Galphai-dependent manner. In addition, CRTH2, but not DP, mediates PGD2-dependent cell migration of blood eosinophils and basophils. Thus, PGD2 is likely involved in multiple aspects of allergic inflammation through its dual receptor systems, DP and CRTH2.

Base Sequence↗
PubMed1985

Blast crisis of chronic granulocytic leukemia with mast cell and basophilic precursors.

The authors report a patient with Ph1-positive chronic granulocytic leukemia (CGL) who developed "blast crisis" after six years of chronic phase. The presence of mast cell precursors and basophil blasts was demonstrated by ultrastructural morphology and cytochemistry. Membrane phenotype studies with monoclonal antibodies helped in the further characterization of these cells. The possible implication of these findings in the origin of mast cells and the relationship of these cells with basophils are discussed.

Adult↗
PubMed1991

Heterogeneity of human mast cells and basophils in response to muscle relaxants.

The authors studied the effects of increasing concentrations 10(-5)-10(-3) M) of four muscle relaxants (succinylcholine, d-tubocurarine, vecuronium, and atracurium) on histamine release from peripheral blood basophils and mast cells isolated from human lung parenchyma, skin tissues, and heart fragments. Basophil granulocytes released less than 5% of their histamine content when incubated with any one of the muscle relaxants tested. In contrast, mast cells showed a significant heterogeneity in response to different muscle relaxants. Succinylcholine did not induce histamine release from any type of mast cell, and only high concentrations of d-tubocurarine (10(-3) M) caused histamine release from skin and lung mast cells. Vecuronium concentration-dependently induced histamine release from skin and lung--but not from heart mast cells--to a maximum of 7.2 +/- 2.1% and 4.9 +/- 1.4%, respectively. Atracurium concentration-dependently caused significant histamine release from skin and lung mast cells to a maximum of 46.2 +/- 15.1% and 30.6 +/- 6.0%, respectively. Atracurium (5 x 10(-5) - 2 x 10(-4) M) also induced histamine release from heart mast cells. The histamine release process from both lung and skin mast cells caused by atracurium and vecuronium was extremely rapid (t1/2 = less than 1 min). The releasing activity of atracurium and vecuronium on lung and skin mast cells was not reduced, and not abolished, by lowering the temperature of the incubation buffer to 22 degrees C and 4 degrees C. Extracellular calcium did not affect the capacity of atracurium and vecuronium to induce histamine release from lung and skin mast cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Basophils↗
PubMed1988

VM-26 (teniposide)-induced hypersensitivity and degranulation of basophils in children.

During a 7 year period, 16 episodes of VM-26 (teniposide) hypersensitivity occurred in our Department of Pediatrics. Eight of these (50%) were observed in neuroblastoma patients, of whom a total of 22 children had been treated with VM-26. The predominant signs were facial edema, flushing, urticaria, bronchospasm, tachycardia, and hypotension. All children with hypersensitivity recovered, but four of them were critically ill. No risk factors were found. In order to elucidate the mechanism of the hypersensitivity episode further, and to identify a possible allergen, histamine release from basophil leukocytes was performed by use of a glass microfiber method. Blood samples from nine cases reacting to VM-26, eight controls (children exposed to VM-26 without any hypersensitivity reactions), and 12 healthy children without previous exposure were challenged with VM-26 alone and with its vehicle, cremaphor. In all samples, it was found that VM-26 degranulated basophils, whereas no histamine release was seen after challenge with cremaphor. The reaction was dose-dependent, and not IgE-mediated, since IgE depletion of the cells did not abolish histamine release after VM-26 challenge.

Adolescent↗
PubMed2000

Mast cells and basophils.

Mast cells and basophils are effector cells in IgE-associated immune responses, such as those that contribute to asthma and other allergic diseases and to host resistance to parasites. Recent work shows that mast cells can also participate in innate immunity to bacterial infection and that the expression of such mast cell-dependent natural immunity can be significantly enhanced by long-term treatment of mice with the kit ligand, stem cell factor. However, mast cells may also influence many other biologic responses, including tissue remodeling and angiogenesis. This review discusses certain recent findings about the differentiation, phenotype, and function of basophils and mast cells, as well as briefly considering evolving concepts about the roles of these cells in health and disease.

Animals↗
PubMed1982

Bullous pemphigoid, an ultrastructural study of the inflammatory response: eosinophil, basophil and mast cell granule changes in multiple biopsies from one patient.

We have studied by electron and light microscopy the inflammatory reaction in lesions at various stages of clinical development from a patient with bullous pemphigoid. The evolution of clinical lesions was associated with a sequence of histopathologic events which began with alterations of mast cells and proceeded to infiltration, first with lymphocytes and later with eosinophils and basophils. Mast cells in the papillary and reticular dermis demonstrated a unique, focal, irregular loss of granule contents. Intact eosinophils demonstrated intracytoplasmic losses of granule contents and karyorrhectic and karyolytic eosinophils had released membranebound granules. Partially and completely degranulated basophils were present within a fibrin gel which formed in the dermis. Thus, the sequence of histopathologic events in the pathogenesis of bullous pemphigoid includes mast cell granule alterations and release of granule contents from eosinophils which are undergoing nuclear and cytoplasmic damage.

Basophils↗
PubMed1983

Erythema multiforme: microvascular damage and infiltration of lymphocytes and basophils.

The sequence of alterations occurring in recurrent erythema multiforme was studied with clinical observations, 1-micrometer tissue sections, and immunofluorescence techniques. Lesions evolved through 3 stages: an initial red papule, a vesicle surmounting a red papule, and a target (iris) lesion. Focal endothelial cell swelling was present in clinically normal skin. In the red papule, endothelial cytoplasmic swelling, vacuolization, and nuclear hypertrophy with luminal obliteration of superficial venules developed. These venular alterations were more marked with endothelial cell necrosis, and involved deeper venules as well in vesicular and target lesions. Lymphocytes surrounded the venules and infiltrated the lower epidermis in the red papule and the vesicular lesions. Venular damage was correlated with the degree of infiltration by lymphocytes, apparently the primary effector cell, suggesting the venule as a primary target of injury. Hypogranulated basophils were noted around venules in vesicular and target lesions. Fibrin deposits were identified within and interstitially beneath the vesicles. The presence of lymphocytes, basophils, and interstitial fibrin deposition is similar to the changes of cutaneous delayed-type hypersensitivity and suggests a role for cell-mediated immunity in the pathogenesis of erythema multiforme.

Adolescent↗
PubMed1980

Basophil mediators and their release, with emphasis on BK-A.

During IgE-mediated events, basophils secrete small molecular weight mediators (histamine, slow reacting substance, Eosinophil chemotactic factor) which are thought to participate in inflammatory processes. We here describe the IgE-mediated secretion of large molecular weight mediators which have the potential for the activation of the Hageman factor dependent pathways, and the generation of biologically active peptides. These large molecular weight basophil derived mediators may, through the activation of the Hageman factor dependent pathways, influence mechanisms which participate in both acute and chronic cell-mediated inflammatory processes. We suggest that these proteases may participate not only as mediators of the immediate hypersensitivity reaction, but may also function in important aspects of the entire inflammatory response.

Autacoids↗
PubMed1978

Recruitment of basophils in delayed hypersensitivity reactions.

Basophilic leukocytes constitute a significant proportion of the cellular infiltrates in many forms of delayed-in-onset hypersensitivity reactions in human beings, guinea pigs, and other animals. In this paper, I review current information on the role of basophils in the reactions, and present similarities and differences between Jones-Mote and classic delayed hypersensitivities.

Animals↗
PubMed1986

The Wiskott-Aldrich syndrome: studies of platelets, basophils and polymorphonuclear leucocytes.

Platelets, basophils and neutrophils from a patient with the Wiskott-Aldrich syndrome (WAS) were exposed to stimuli that activate specific membrane receptor or directly initiate biochemical events (e.g. the Ca2+ ionophore A23187 and ionomycin or arachidonic acid). Platelets from this patient did not aggregate in response to ADP, collagen, thrombin or adrenaline, which activate specific membrane receptors. Platelet aggregation, however, was normal in response to compound A23187, ionomycin or exogenous arachidonic acid. Histamine release from basophils of the WAS patient was normal in response to anti-IgE, a formylated peptide (f-met peptide), and to A23187. Similarly, the release of the lysosomal enzymes, beta-glucuronidase and lysozyme, from neutrophils of the WAS patient in response to serum treated zymosan (Zx), f-met peptide, and A23187 was not significantly different from that of his parents and 13 normal donors. These results suggest that the primary defect in WAS is selectively present in platelets and is located in a biochemical step between receptor activation and Ca2+ influx and/or initiation of arachidonate metabolism.

Arachidonic Acid↗
PubMed1994

Marked basophilia in acute promyelocytic leukaemia treated with all-trans retinoic acid: molecular analysis of the cell origin of the basophils.

We report a patient with acute promyelocytic leukaemia who developed marked basophilia during all-trans retinoic acid treatment. We studied genomic DNA and RNA extracted from the patient's peripheral leucocytes in order to determine the origin of the basophils. The RAR alpha rearranged band in the Southern blot analysis and a chimaeric product of PML-RAR alpha by polymerase chain reaction were strongly visible before ATRA treatment, but at the time of maximal basophilia both of them were markedly diminished. These findings suggest that the basophils which appeared during the ATRA treatment are reactive in nature rather than a leukaemic clone.

Base Sequence↗
PubMed1980

The in vitro effect of levamisole on lymphocyte proliferation, polymorphonuclear leucocyte chemotaxis, basophil histamine release and platelet serotonin release in patients with atopic dermatitis.

The in vitro effect of levamisole (LMS) on lymphocyte, neutrophil, basophil and platelet function was investigated in patients with severe atopic dermatitis and hyperimmunoglobulinaemia E. Lymphocyte stimulation by several concentrations of PHA, con A and PWM, polymorphonuclear leukocyte chemotaxis and basophil histamine release were unaffected by LMS (10 micrograms/ml). Platelet serotonin release induced by iodipamide was decreased in patient and control groups by LMS but release induced by methacholine, epinephrine and thrombin was not.

Basophils↗
PubMed1982

Allergen-specific IgE and IgG4 antibody levels in sera and the capacity of these sera to sensitize basophil leucocytes in vitro.

Leucocytes from normal non-allergic donors were passively sensitized with sixty-five atopic sera that contained IgE directed against house dust mite (HDM) or guinea-pig dander (GPD). In no serum was there any IgE with an abnormal basophil anaphylactic-sensitizing activity. In sera from patients hypersensitive to GPD, both GPD-specific IgE and IgG4 were measured. A significant correlation was found between the GPD-IgE RAST and the basophil-sensitizing capacity of GPD-positive sera, but no correlation was found between this sensitizing capacity and the GPD-IgG4 RAST. Leucocytes were passively sensitized with serum mixtures that contained the same amounts of total and HDM-specific IgE; these mixtures differed as to sensitizing activity. It is unclear whether this variation is due to differences in IgE or to influences of other factors in serum.

Allergens↗
PubMed1984

Plasma of normal, but not atopic persons reducing basophil degranulation induced by anti-IgE.

The response to anti-IgE serum of basophils from allergic and normal persons in the presence of whole plasma or as washed cells in Tyrode solution was examined to detect any inhibiting activity of human plasma. A factor reducing the potential of anti-IgE serum to degranulate basophils was present in plasma of normal but not of allergic persons. It is considered that this property of plasma could contribute to homeostatic control in immediate hypersensitivity.

Adult↗