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  • 1
    Electronic Resource
    Electronic Resource
    Anti-inflammatory effects of glucocorticoids and cyclosporin A on human basophils (1993)
    Springer
    European journal of clinical pharmacology 45 (1993), S. S17 
    Details
    ISSN: 1432-1041
    Keywords: Basophils ; Cyclosporin A ; Corticosteroids ; deflazacort ; histamine ; leukotriene C4
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Pro-inflammatory and vasoactive mediators released from human basophils and mast cells play a role in several inflammatory and immune disorders. It was recently demonstrated that cyclosporin A (CsA) exerts anti-inflammatory effects by inhibiting the release of preformed and de novo synthesized mediators from human basophils [1]. This study compared the effects of pharmacological concentrations of deflazacort (DFZ) and prednisolone (PRED) on the anti-IgE-mediated release of preformed (histamine) and de novo synthesized (leukotriene C4: [LTC4]) mediators from basophils. Basophils were cultured for 18 hours in the presence of pharmacological concentrations of DFZ (10−8 to 3 × 10−6 M). DFZ inhibited the anti-IgE-mediated release of histamine and LTC4 from basophils in a concentration-dependent manner (6–40 %), and had a similar efficacy and potency to PRED. The effect of DFZ (10−8 to 10−8 M) in combination with CsA on the immunological release of histamine and LTC4 from basophils was also evaluated. An 18-hour incubation of basophils with DFZ (10−8 M) followed by a short (15-minute) incubation with CsA (30 ng/ml) resulted in an additive inhibition of the release of histamine and LTC4. The additive anti-inflammatory effect of these drugs makes them interesting candidates for future controlled clinical trials in inflammatory diseases in which basophil-derived mediators play a relevant role.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01844198
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  • 2
    Electronic Resource
    Electronic Resource
    Assessment of signal transducer and activator of transcription 6 as a target of glucocorticoid action in human airway epithelial cells (2004)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 34 (2004), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Activation of signal transducer and activator of transcription (STAT)6 by IL-4 and IL-13 is essential in many key epithelial responses in the asthmatic airway including expression of numerous chemokines, goblet cell differentiation and mucus production and expression of other allergic inflammatory genes. While these responses are all inhibited by glucocorticoids (GC) administered systemically or by inhalation, the inhibitory mechanisms are unknown.Objective To test the hypothesis that GC suppress allergic responses by blocking IL-4-induced STAT6 signalling in airway epithelial cells.Methods Western blotting and reporter gene assays were used to determine whether GC could inhibit STAT6 production, phosphorylation or nuclear translocation, or whether GC could affect STAT6 transcriptional activity in the BEAS-2B airway epithelial cell line.Results Our results showed that GC had no inhibitory effect on the total cellular or nuclear levels of STAT6 or phospho-STAT6. GC did not inhibit transcription from three different STAT6-driven reporter constructs, indicating that GC also did not inhibit STAT6 function.Conclusion We conclude that airway epithelial STAT6 is not the central target of GC in allergic inflammation and that the inhibitory effect of GC on STAT6-mediated IL-4- and IL-13-induced responses is exerted by targeting pathways distinct from STAT6.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2004.02091.x
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  • 3
    Electronic Resource
    Electronic Resource
    Pathophysiology of contrast media anaphylactoid reactions: new perspectives on an old problem (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 53 (1998), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1998.tb03829.x
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  • 4
    Electronic Resource
    Electronic Resource
    Selective activation of human mast cells by general anesthetics (1992)
    Springer
    Inflammation research 36 (1992), S. C191 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated thein vitro effects of increasing concentrations of three general anesthetics commonly used in clinical practice, i.e., ketamine (10−6–10−3 M), thiopentone (10−5–8×10−4 M) and propofol (5–70 μg/ml), on histamine release (HR) from human peripheral blood basophils and mast cells isolated from lung parenchyma (HLMC) and skin tissues (HSMC). None of the drugs induced HR from basophils. Ketamine caused HR from HLMC (p〈0.001 compared to spontaneous release [SR]) and HSMC (p〈0.05 compared to SR). Thiopentone induced limited HR from HLMC (p〈0.05 compared to SR). Propofol induced HR from HLMC (p〈0.005 compared to SR) and HSMC (p〈0.05 compared to SR). Thus, general anesthetics induce HR selectively from human mast cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01997330
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  • 5
    Electronic Resource
    Electronic Resource
    Heterogeneity of human basophils and mast cells in response to muscle relaxants (1992)
    Springer
    Inflammation research 36 (1992), S. C195 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated thein vitro effects of increasing concentrations (10−5–10−3 M) of four muscle relaxants (succinylcholine, d-tubocurarine, vecuronium and atracurium) on histamine release (HR) from human peripheral blood basophils and mast cells isolated from lung parenchyma (HLMC) and skin tissues (HSMC). Basophils released less than 5% of their histamine content when incubated with any one of the muscle relaxants. In contrast, mast cells showed a marked heterogeneity in their response. Succinylcholine did not induce HR from any type of mast cell, and only high concentrations of d-tubocurarine (10−3 M) caused HR from HSMC and HLMC. Vecuronium concentration-dependently induced HR from HLMC and HSMC. Atracurium concentration-dependently caused marked HR from HLMC and HSMC up to a maximum of 46.2±15.1% and 30.6±6.0%, respectively. From both HLMC and HSMC HR caused by atracurium and vecuronium was extremely rapid (t1/2〈1 min). The releasing activity of atracurium and vecuronium on HLMC and HSMC was reduced, but not abolished, by lowering the temperature of the incubation buffer to 22°C and 4°C. These results confirm that there are functional differences between human basophils and mast cells and among mast cells isolated from different anatomical sites in response to the muscle relaxants tested.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01997331
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  • 6
    Electronic Resource
    Electronic Resource
    Inhibition of histamine release from human FcεRI+ cells by nimesulide (1992)
    Springer
    Inflammation research 36 (1992), S. C311 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously demonstrated that pharmacological concentrations of non-steroidal anti-inflammatory drugs (NSAID) such as indomethacin, acetylsalicylic acid, and meclofenamic acid enhance IgE-mediated histamine release (HR) from human basophils. We have now examined the effects of nimesulide (NIM), a new NSAID, on mediator release from human basophils. Preincubation (10 min at 37°C) of basophils with pharmacological concentrations (10−6−10−3 M) of NIM resulted in a concentration-dependent decrease of HR induced by anti-IgE, the Ca2+-ionophore A23187 and the formylated tripeptide f-Met-Leu-Phe (FMLP). Maximal inhibition of anti-IgE-induced HR was achieved after preincubation with 10−4 M NIM and ranged between 14.5% and 44.5% (mean±SEM, 29.7±4.5%). The drug had a marked inhibitory effect on HR from basophils induced by A23187 (80.6±5.5%), FMLP (63.5±10.3%), 12-O-tetradecanoyl-phorbol-13-acetate (57.0±8.7%) and bryostatin 1 (65.7±7.6%). NIM also inhibited the IgE-mediated synthesis of peptide leukotriene C4 from basophils.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01997360
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