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At least 667 records · Page 37Linked to original sources
PubMed1997

Inhibition of allergen-induced histamine release from human basophils by cyclosporine A and FK-506.

A number of structurally different allergens trigger the release of mediators from basophils by cross-linking of IgE receptors. In this study, we analyzed the effects of cyclosporine A (CSA) and FK-506 on allergen-induced histamine release in human blood basophils obtained from birch- or grass-pollen-allergic donors (n = 12). Preincubation of basophils with CSA (0.003-3 microg/ml) or FK-506 (0.003-3 microg/ml) led to inhibition of histamine release induced by purified recombinant tree pollen allergens (r Bet v 1, r Bet v 2) and timothy grass pollen allergens (r Ph1 p 1, r Ph1 p 2, r Ph1 p 5). The effects of CSA and FK-506 were dose dependent, with IC50 values ranging between 0.03 and 0.3 microg/ml for both CSA and FK-506. Cyclosporine H, an inactive CSA analog, did not show any effect on allergen-induced histamine secretion. IgE dependency of the reaction was demonstrated in passive transfer experiments using highly enriched human basophils (> 95% pure) and specific IgE from a patient allergic to Bet v 2. In summary, our data show that CSA and FK-506 inhibit recombinant-allergen-induced histamine release from peripheral blood basophils in allergic donors.

Adult↗
PubMed1978

Mast cell leukemia and acute basophilic leukemia. Cytochemical studies.

Human mast cells and basophil granulocytes can be easily recognized in normal tissues by light microscopy. In one mast cell and one basophilic leukemic case considered in this study, mast cells and basophils were morphologically quite similar and could not therefore be clearly defined merely by their morphological features. Both types of cells showed round nuclei and deep purple granules. The diagnosis of mast cell leukemia or basophilic leukemia was made on the basis of different cytochemical patterns. In the case of mast cell leukemia, peroxidase and PAS stains were negative, while chloroesterase was strongly positive; in the case of basophilic leukemia, peroxidase and PAS stains were positive, while chloroesterase reaction showed a peculiar pattern. Toluidine blue metachromasia and astra blue positivity were present in the cells of both cases.

Basophils↗
PubMed2001

Segmental bronchoprovocation in allergic rhinitis patients affects mast cell and basophil numbers in nasal and bronchial mucosa.

Mast cells and basophils are cells that play an important role in the initiation and control of allergic inflammation in asthma and rhinitis. This study was undertaken to determine the presence and dynamics of mast cells and basophils in the nasal and bronchial mucosa of allergic rhinitis patients after segmental bronchial provocation (SBP). Eight nonasthmatic, grass pollen-allergic rhinitis patients and eight healthy controls were included. Bronchial and nasal biopsies, as well as blood samples, were taken before (T(0)) and 24 h (T(24)) after SBP. Immunohistochemical staining was performed for mast cells (tryptase and chymase; phenotypes MC(T), MC(TC), MC(C)) and basophils (BB1). In the bronchial mucosa, the number of BB1(+) cells increased significantly (p < 0.05) in allergic rhinitis patients after SBP. In the nasal mucosa, the numbers of MC(C) and MC(TC) cells decreased significantly, whereas the numbers of [BB1(+)] cells increased significantly in allergic rhinitis patients after SBP (p < 0.05). In blood, the number of basophils decreased (p < 0.05) and the level of interleukin (IL)-5 increased (p < 0.05) in atopic patients after SBP. No significant changes could be observed in healthy controls. This study shows that SBP in nonasthmatic allergic rhinitis patients reduces numbers of mast cells in the nose as a result of enhanced degranulation. At the same time, there is evidence for an influx of basophils from the blood into the nasal and bronchial mucosae.

Adolescent↗
PubMed1994

Identification of IgE-bearing cells in the late-phase response to antigen in the lung as basophils.

We have carried out studies to ascertain whether the histamine-containing, IgE-bearing cells found in the bronchoalveolar lavage (BAL) fluid obtained during the late-phase response following subsegmental antigen challenge of human airways are predominantly basophils or mast cells. Four lines of evidence suggest that most are basophils: (1) The cells fulfill morphologic criteria for light microscopy. (2) Cell surface markers determined by immunofluorescence and flow cytometry revealed that the IgE-bearing cells express the leukocyte antigens Fc gamma RII and the beta 2 integrins, LFA-1 and Mac-1, but do not express the mast cell-associated c-kit receptor for stem cell factor. (3) The late-phase histamine-containing cells in late-phase BAL fluids have the functional characteristics of basophils in their secretory responses to anti-IgE, the f-met peptide, and phorbol ester TPA. (4) The cells have a functional histamine type 2 receptor, a characteristic of basophils, not mast cells. We conclude that basophils infiltrate the lower airways hours after antigen exposure. These cells may be responsible for the mediator release observed at that time.

Alcian Blue↗
PubMed1992

Interleukin-8 and RANTES inhibit basophil histamine release induced with monocyte chemotactic and activating factor/monocyte chemoattractant peptide-1 and histamine releasing factor.

The objective of this study was to investigate the effect of interleukin-8 (IL-8) and RANTES on basophil histamine release induced with monocyte chemoattractant peptide-1 (MCP-1) and crude histamine releasing factor (HRF). IL-8 induced low levels of histamine release (8.5 +/- 0.5%) from basophils obtained from only six of 20 donors at high concentrations (10(-6) M). RANTES induced histamine release (16 +/- 2%) from basophils of four of 15 donors at 10(-7) M concentration. However, both IL-8 and RANTES inhibited MCP-1 and HRF-induced histamine release from basophils dose-dependently at concentrations of 10(-9) to 10(-7) M. Basophils from all donors showed a significant inhibitory response (greater than 15%). The maximal inhibition of MCP-1 and HRF by IL-8 was 28 +/- 4% and 48 +/- 8%, respectively. The maximal inhibition of MCP-1 and HRF by RANTES was 26 +/- 4% and 43 +/- 6%, respectively. Peripheral blood mononuclear cell-derived HRF was purified into three distinct peaks by reverse-phase high performance liquid chromatography. Peak I contained MCP-1 as judged by binding to an immunoaffinity column that was prepared with anti-MCP-1 antibody. IL-8 inhibited histamine release induced with all three peaks of HRF. The inhibition of histamine release by IL-8 was significantly higher in normal subjects than in allergic patients (59 +/- 9% versus 31 +/- 7%, P less than 0.05). Both IL-8 and RANTES inhibited cytokine-induced histamine release only and did not affect histamine release by anti-IgE, FMLP, and C5a.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Infective Agents↗
PubMed1992

Role of tyrosine kinases in IgE-mediated signal transduction in human lung mast cells and basophils.

Recent evidence suggests that tyrosine kinases play an important role in signal transduction mechanisms utilized by a range of different agonists in many cell types. We have investigated the effects of four different inhibitors of tyrosine kinases on IgE-dependent histamine release from human lung mast cells and basophils. Genistein inhibited the anti-IgE-induced histamine release from human basophils (at 10 microM genistein, inhibition = 55 +/- 5%, n = 17, P < 0.005) with an IC50 of 8 microM, but was much less effective in the human lung mast cell (at 10 microM, inhibition = 18 +/- 6%, n = 11, P < 0.05). Two inactive analogs of genistein, genistin and diadzein, failed to affect anti-IgE-induced histamine release significantly in either mast cells or basophils. A second inhibitor of tyrosine kinases, tyrphostin 25, inhibited IgE-dependent release from basophils (at 10 microM, inhibition = 25 +/- 7%, n = 6, P < 0.05) though it was less effective than genistein and failed to affect IgE-induced histamine release from human lung mast cells (at 10 microM, inhibition = 22 +/- 16%, n = 5, P = NS). In contrast, methyl 2,5 dihydroxycinnamate (MDC) failed to inhibit anti-IgE-dependent histamine release in human basophils (at 10 microM, inhibition = 3 +/- 3%, n = 5, P = NS) but proved to be an effective inhibitor of anti-IgE-induced degranulation in human lung mast cells (at 10 microM, inhibition = 53 +/- 16%, n = 5, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Basophils↗
PubMed1994

Charcot-Leyden crystal protein distribution in basophils and its absence in mast cells that differentiate from human umbilical cord blood precursor cells cultured in murine fibroblast culture supernatants or in recombinant human c-kit ligand.

Suspension cultures of human umbilical cord blood mononuclear cells supplemented with c-kit ligand-containing additives give rise to a mixture of cells belonging to several lineages. Among those that differentiate in quantity are mature basophils, immature mast cells, and neutrophilic myelocytes. We used an ultrastructural immunogold method to detect the Charcot-Leyden crystal (CLC) protein, an eosinophil- and basophil-specific protein, to study cells that were obtained at sequential times from 3 to 14 weeks in culture. Basophils (and eosinophils, which were present in smaller numbers) labeled for the CLC protein; mast cells did not. The labeled basophil subcellular sites included formed intragranular, cytoplasmic and nuclear CLCs, cytoplasmic particle-filled and homogeneously dense granules, cytoplasm, nucleus, plasma membrane, and cytoplasmic and Golgi area vesicles. Individual basophil ultrastructural phenotypes similar to those associated with stimulated release and recovery reactions showed the expected variations in the gold-labeled subcellular compartments. Macrophages also were labeled for CLC protein within endocytotic-lysosomal structures; neutrophilic myelocytes did not contain CLC protein. On the basis of findings reported here, the combined ultrastructural morphology and immunogold phenotyping of cells differentiating in c-kit ligand-supplemented cultures allows accurate lineage assignment of the developing cells.

3T3 Cells↗
PubMed2006

Granzyme B, a novel mediator of allergic inflammation: its induction and release in blood basophils and human asthma.

Histamine, leukotriene C4, IL-4, and IL-13 are major mediators of allergy and asthma. They are all formed by basophils and are released in particularly large quantities after stimulation with IL-3. Here we show that supernatants of activated mast cells or IL-3 qualitatively change the makeup of granules of human basophils by inducing de novo synthesis of granzyme B (GzmB), without induction of other granule proteins expressed by cytotoxic lymphocytes (granzyme A, perforin). This bioactivity of IL-3 is not shared by other cytokines known to regulate the function of basophils or lymphocytes. The IL-3 effect is restricted to basophil granulocytes as no constitutive or inducible expression of GzmB is detected in eosinophils or neutrophils. GzmB is induced within 6 to 24 hours, sorted into the granule compartment, and released by exocytosis upon IgE-dependent and -independent activation. In vitro, there is a close parallelism between GzmB, IL-13, and leukotriene C4 production. In vivo, granzyme B, but not the lymphoid granule marker granzyme A, is released 18 hours after allergen challenge of asthmatic patients in strong correlation with interleukin-13. Our study demonstrates an unexpected plasticity of the granule composition of mature basophils and suggests a role of granzyme B as a novel mediator of allergic diseases.

Antibodies, Monoclonal↗
PubMed1996

Defective inhibition of sodium on basophil histamine release in patients with allergic rhinitis and bronchial asthma.

The aim of this study was to evaluate whether Na+ exerts its inhibitory effect on basophil histamine release induced by immunoglobulin E (IgE)-dependent (anti-IgE) and IgE-independent (N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-3 (IL-3)) stimuli in patients with allergic rhinitis (n = 24) and allergic bronchial asthma (n = 10). Peripheral blood leucocytes were stimulated with anti-IgE, FMLP and IL-3 in the presence of high and low Na+ concentrations, and histamine release was measured using a fluorometric method. In standard Na(+)-containing medium, spontaneous and stimulated histamine release was higher in allergic patients (n = 34) (both rhinitic and asthmatic) than in healthy subjects (n = 41). Na+ removal from extracellular medium and its isosmotic substitution with choline chloride or with N-methyl-D-glucamine led to a significant increase of anti-IgE-, FMLP- and IL-3-induced histamine release in normal subjects, but not in allergic patients. The increase in Na+ concentration in the extra-cellular medium was accompanied by a dose-dependent decrease of anti-IgE- and FMLP-induced histamine release in normal subjects, but not in allergic patients. The behaviour of atopics and healthy subjects was different and not related to the basophil responsiveness to activating signals. The incubation of basophils from healthy subjects with sera from allergic patients did not have a significant influence on the inhibitory effect of Na+. Basophils from healthy subjects and atopic patients respond differently when stimulated in a low Na+ medium. The reduced sensitivity to the inhibitory effect of Na+ may contribute to basophil dysfunction in patients with respiratory allergy.

Adult↗
PubMed2000

Mast cells and basophils in acquired immunity.

In this review we describe the basic biology of mast cells and basophils and discuss their proposed effector and immunoregulatory roles in acquired immunity, particularly the IgE-associated immune responses. While mast cells and basophils share a number of similarities, they also differ in many aspects of natural history and function. Both mast cells and basophils express the high affinity receptor for immunoglobulin E (Fc epsilon RI) on their surface and can be activated to secrete diverse preformed, lipid and cytokine mediators after crosslinking of Fc epsilon RI-bound IgE with bi- or multivalent antigen. Thus, both cell types can represent important effector cells, as well as potential immunoregulatory cells, in IgE-mediated acquired immunity. However, mature mast cells are long-term residents of vascularized tissues, whereas basophils are granulocytic leukocytes that circulate in mature form and must be recruited into tissues that are sites of inflammatory or immune responses. The similarities and differences in the natural history, mediator content and other features of mast cells and basophils not only strongly indicate that these cells represent distinct hematopoietic lineages that can express complementary or overlapping functions, but also offer insights into the specific roles of these cells in acute, 'late phase' and chronic aspects of adaptive or pathological IgE-associated acquired immune responses.

Acute Disease↗
PubMed1998

Effect of radiographic contrast media on histamine release from human mast cells and basophils.

Radiographic contrast media (RCM) cause histamine-dependent allergic-like reactions. The direct effects of diatrizoate (high osmolar ionic monomer), ioxaglate (low osmolar ionic dimer), iopromide (low osmolar non ionic monomer) and iotrolan (iso-osmolar non ionic dimer) at the concentration of 200 mgI ml-1 (60 min exposure) on the release of histamine from human basophils, human lung mast cells (HLMC), and human skin mast cells (HSMC) were investigated. Diatrizoate induced 48 +/- 4% histamine release in basophils, 15 +/- 3% in HLMC and 25 +/- 6% in HSMC. The remaining RCM were relatively ineffective activators of histamine release in both HLMC and HSMC (ioxaglate 4 +/- 1% and 4 +/- 1%, iopromide 5 +/- 1% and 7 +/- 2%, iotrolan 7 +/- 2% and 10 +/- 3%, respectively). Both iotrolan and ioxaglate were effective in basophils inducing 21 +/- 3% and 24 +/- 6% histamine release, respectively, whereas iopromide was relatively ineffective (7 +/- 4%). Diatrizoate induced histamine release from all three cell types with optimal levels of histamine release after a 2-4 h incubation although significant levels occurred within 15 min. Dose-dependent histamine release from HLMC occurred in all four types of RCM, the largest response (37 +/- 3%) being produced by diatrizoate. The effect of osmolality on histamine release was investigated using different concentrations of mannitol solutions (0.25, 0.5 and 1 M). Histamine release from HLMC, HSMC and basophils after 90 min exposure to mannitol (1 M) was 24 +/- 2% (p < 0.05), 9 +/- 3% (p = 0.06) and 49 +/- 1% (p < 0.05), respectively, suggesting that hyperosmolality per se can induce histamine release from basophils and mast cells. Diatrizoate-induced histamine release in all three cell types was significantly reduced by lowering the temperature to 0 degree C and partially attenuated by the metabolic inhibitors antimycin A (1 microM) and 2-deoxyglucose (5 mM), and by the omission of glucose from the buffer solution. Diatrizoate-induced histamine release was not dependent on extracellular calcium. These data suggest that diatrizoate induces histamine release at least in part by non-cytotoxic mechanisms.

Basophils↗
PubMedDate not supplied

Basophilic crisis of chronic myelogenous leukemia.

An 81-year-old woman with Ph1-positive chronic myelogenous leukemia developed blast crisis four years after diagnosis of the disease. In the blast crisis phase, hematological examination disclosed WBC 93,000/microliters with basophilia in both the peripheral blood (40.0%) and bone marrow (33.2%), with increased numbers of immature basophils, such as basophilic promyelocytes, myelocytes and metamyelocytes. Electron microscopy of bone marrow cells showed immature and mature types, which contained granules characteristic of basophils. Toluidine blue metachromasia was evident in the basophils. Cytogenetic study revealed the Ph1 chromosome along with additional abnormalities. In view of these findings, it seems likely that basophilic crisis developed in this patient with chronic myelogenous leukemia.

Aged↗
PubMedDate not supplied

Anaphylaxis caused by cloxacillin: diagnosis with seriated analysis by way of basophil activation test.

We report a case of anaphylaxis caused by cloxacillin in a 13-year-old patient. The basophil activation test, performed 25 days after the anaphylactic reaction, was positive to cloxacillin, amoxicillin, and penicillin G and negative to ibuprofen, tolerated by the patient. The analysis was performed 17 days after the reaction was not conclusive because 74% of the basophil population was activated in basal conditions. The abnormally high activation was similar to that found in an analysis before the reaction, exactly 4 days after finishing a well-tolerated treatment with amoxicillin. This first analysis was available because a patient's sample was taken from the emergency laboratory as a blind control for a study to assess the basophil activation test reliability in diagnosis of hypersensitivity to NSAIDs. The high number of activated basophils in basal conditions after treatment with amoxicillin and before the anaphylactic reaction to cloxacillin probably reflects the beginning of the sensitization. Until now, no cases of hypersensitivity to cloxacillin have been diagnosed by means of the basophil activation test.

Adolescent↗
PubMed2001

Differences in functional consequences and signal transduction induced by IL-3, IL-5, and nerve growth factor in human basophils.

Previous studies have indicated a redundancy in the effects of the cytokines, IL-3, IL-5, and nerve growth factor (NGF) on acute priming of human basophils. In the current study, we have examined the effects of these three cytokines on 18-h priming for leukotriene C4 generation, their ability to induce Fc(epsilon)RIbeta mRNA expression, or their ability to sustain basophil viability in culture. We also examine a variety of the signaling steps that accompany activation with these cytokines. In contrast with the ability of IL-3 to alter secretagogue-mediated cytosolic calcium responses following 18-h cultures, 18-h treatment with IL-5 or NGF did not affect C5a-induced leukotriene C4 generation or alter C5a-induced intracellular Ca2+ concentration elevations. IL-3 and IL-5, but not NGF, induced Fc(epsilon)RIbeta mRNA expression and all three improved basophil viability in culture with a ranking of IL-3 > IL-5 > or = NGF. All three cytokines acutely activated the extracellular signal-regulated kinase pathway and the signaling elements that preceded extracellular signal-regulated kinase and cytosolic phospholipase A2 phosphorylation, consistent with their redundant ability to acutely prime basophils. However, only IL-3 and IL-5 induced Janus kinase 2 and STAT5 phosphorylation. This pattern of signal element activation among the three cytokines most closely matched their ability to induce expression of Fc(epsilon)RIbeta mRNA. Induction of the sustained calcium signaling that follows overnight priming with IL-3 appeared to be related to the strength of the early signals activated by these cytokines but the relevant pathway required was not identified. None of the signaling patterns matched the ability of the cytokines to promote basophil survival.

Adjuvants, Immunologic↗
PubMed2001

Chemokine receptors in human basophils: inducible expression of functional CXCR4.

We examined the expression profile of chemokine receptors in human basophils and their regulation by cytokines. Basophils expressed transcripts of CC chemokine receptors (CCR)1, CCR2, CCR3, and CCR5 and CXC chemokine receptors (CXCR)1, CXCR2, and CXCR4. In contrast to the other receptors, surface-CXCR4 expression was not detected in fresh- and whole-blood basophils, but it became apparent gradually during incubation. Among 16 chemokines tested, eotaxin induced the most potent basophil migration. SDF-1 also induced a strong, migratory response comparable with that induced by eotaxin in 24-h, cultured basophils, but it failed to induce degranulation. IL-3 abrogated CXCR4 expression completely, and it only down-regulated CCR2 and CCR3 expression slightly. IL-5, GM-CSF, and IL-4 also down-regulated CXCR4 expression. Thus, expression of CXCR4 was the most strongly affected by cytokines, and this may represent an alternative mechanism for control of cell-specific, biological responses to SDF-1.

Basophils↗
PubMed2002

Regulation of mediator secretion in human basophils by p38 mitogen-activated protein kinase: phosphorylation is sensitive to the effects of phosphatidylinositol 3-kinase inhibitors and calcium mobilization.

Although human basophils modulate allergic diseases by secreting histamine, leukotriene C(4), interleukin (IL)-4, and IL-13, the intermediary signals controlling the release of these mediators are poorly understood. Here, we show that p38 mitogen-activated protein kinase (MAPK) crucially affects basophil activation following stimulation with various secretagogues. Phosphorylation of p38 MAPK occurred within 5 min following anti-immunoglobulin (Ig)E stimulation, but was more rapidly activated in basophils stimulated with formyl-Met-Leu-Phe or A23187. Additionally, activation of p38 MAPK to the above stimuli was dependent on extracellular influx and intracellular mobilization of calcium. SB 203580, a specific p38 MAPK inhibitor, blocked anti-IgE-induced secretion of all basophil mediators and reduced not only p38 MAPK, but also extracellular signal-regulated kinases 1 and 2 activity, whereas the MAPK antagonist, PD 098059, did not affect p38 MAPK. IgE-dependent activation of p38 MAPK and MKK3/6 was affected by LY 294002 and wortmannin, suggesting that these kinases are targets for phosphatidylinositol 3 kinase (PI 3-K). We conclude that p38 MAPK is a pivotal regulator of basophil function downstream of PI 3-K activation and calcium mobilization.

Albuterol↗
PubMed2004

Basophil activation and sulfidoleukotriene production in patients with immediate allergy to betalactam antibiotics and negative skin tests.

BACKGROUND: New in vitro diagnostic methods for IgE-mediated drug allergic reactions, such as basophil activation test and antigen specific sulfidoleukotriene test, have proven their usefulness in patients with positive skin tests. OBJECTIVE: To assess the usefulness of basophil activation test and antigen specific sulfidoleukotriene test in the diagnosis of patients with IgE-mediated allergy to Betalactam antibiotics and negative skin tests. METHODS: The 23 patients included in the study underwent basophil activation test, antigen specific sulfidoleukotriene test and specific IgE. The patients were classified into three groups. GROUP A: patients with positive specific IgE. GROUP B: patients with a unique immediate reaction to Betalactams, negative specific IgE and positive oral provocation tests. And Group C: patients with at least two immediate reactions induced by Betalactams and negative specific IgE. RESULTS: The sensitivity/specificity of the different tests are: basophil activation test 39.1 %/93.3%, antigen specific sulfidoleukotriene test 22.7%/83.3%, specific IgE 21.7%/86.7%. The joint use of the three tests allows diagnosis of 60.9% of the patients. CONCLUSION: In vitro diagnostic tests, especially basophil activation test, are very important tools in the diagnosis of patients with IgE-mediated allergy to Betalactams and negative skin tests, avoiding performance of potentially dangerous oral provocation tests in a high percentage of cases.

Adult↗
PubMed2005

[Histamine release properties of human basophils in response to various stimuli].

AIM: To investigate the effects of protease activated receptor-2 (PAR-2) agonist, heparin and other stimuli on histamine release from human basophils. METHODS: Peripheral blood mononuclear cells (PBMCs) were separated by density gradient centrifugation. The PBMCs were then resuspended in complete Hank's balanced salt solution (HBSS) and challenged with various stimulating agents. Histamine level in samples was determined by ELISA. RESULTS: 10 mg/L trypsin could induce histamine release from basophils. However, its stimulatory effect on basophils was weaker than that of anti-IgE, calcium ionophore (CI), F-Met-Leu-Phe (FMLP), C5a and substance P. PAR-2 agonist SLIGKV-NH(2) failed to activate basophils. Heparin, C5 and adenosine did not induce any histamine release at concentrations tested, but heparin enhanced histamine release induced by C5a and substance P. CONCLUSION: Trypsin, anti-IgE, CI, FMLP, C5a and substance P can induce histamine release from baosophils, but PAR-2 agonist can not. Heparin can greatly enhance the ability of C5a and substance P to stimulate histamine release, which may be a novel mechanism of amplification of basophil activation signal.

Animals↗