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  • 1
    Electronic Resource
    Electronic Resource
    The Bronchoconstrictor Effect of Sensory Neuropeptides in Man (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 629 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb37990.x
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  • 2
    Electronic Resource
    Electronic Resource
    Genetic control of indirect airway responsiveness in the rat (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 25 (1995), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Many of the airway responses to endogenous and exogenous stimuli are caused by indirect mechanisms such as the activation of neurons and/or inflammatory cells. In the present study we compare the bronchoamstrictor and the plasma protein extravasation response to adenosine and tachykinins in two highly inbred rat strains. F344 and BDE. BDE-rats have a bronchoconstrictor response to adenosine at lower doses. Challenge with the A3-adenosine receptor agonist APNEA demonstrates that the difference in airway responsiveness to adenosine between BDE- and F344-rats is probably related to a higher number of A3-receptors on the airway mast cells of BDE-rats. In contrast. F344-rats have a higher airway responsiveness to lachykinins than BDE-rats. Taehykinins cause bronchoconstriction in F344-rats mainly by an indirect mechanism, involving stimulation of NK1-receptors and mast cell activation. In BDE-rats they cause bronchoconstriction by a direct effeet on airway smooth muscle via activation of NK2-receptors. Finally we also observed a difference between F344-and BDE-rats with regard to the mechanisms involved in the plasma protein extravasation in the airways caused by substance P or capsuicin. In K344-rats but not in BDE-rats mast cell activation and the release of 5-hydroxytryptamine is partly responsible for this plasma protein extravasation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1995.tb00423.x
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  • 3
    Electronic Resource
    Electronic Resource
    The effect of zardaverine, an inhibitor of phosphodiesterase isoenzymes III and IV, on endotoxin-induced airway changes in rats (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 23 (1993), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Zardaverine is a novel phosphodiesterase III/IV inhibitor, developed as a potential therapeutic agent for asthma. In this study we evaluated the effect of zardaverine in an in vivo animal model of airway inflammation and hyperresponsiveness. Endotoxin exposure in rats causes a transient increase in airway responsiveness and a neutrophilic inflammation of the bronchi, which are both at least partly mediated through the secondary release of tumour necrosis factor a (TNFα), Groups of 10 animals each were pretreated with placebo or zardaverine (1, 10, 30μmol/kg) i.p., 30 min prior to exposure to aerosolized endotoxin (LPS) or saline. Ninety minutes later, airway responsiveness to 5-HT was assessed and bronchoalveolar lavage (BAL) performed. Zardaverine did not influence basehne lung resistance (RL), but inhibited dose dependently the 5-HT induced increase in RL in control animals. In placebo pretreated animals LPS exposure caused a signiflcant decrease in PC50RL5-HT (provocative concentration of 5-HT causing a 50% increase in RL), compared to the saline exposed control group (1.1 ± 0.1 vs 2.7± 0.4μg/kg) (P〈0.01). This decrease in PC50RL-HT was significantly inhibited by zardaverine 30μmol/kg (5.4 ± 1.8 vs 1.1 ± 0.1μg/kg) (P〈0.05). Compared to placebo pre-treated, LPS exposed animals, zardaverine 30 μmol/kg also significantly inhibited to LPS induced neutrophil increase (193.0 ± 50.0 vs 915.6± 181.3 × 103) (P 〈 0.05), increase in elastase activity (23 ± 11 vs 54 ± 9 nmol substrate/h/ml) (P〈0.05) and TNFα release in BAL fluid (93.1 ± 19.5 vs 229.5 ± 24.8 U/ml BAL fluid) (P〈0.01).These results indicate that zardaverine suppresses the endotoxin indueed airway inflammation and hyperresponsiveness in rats. Protection against the increase in responsiveness can be attributed both to inhibition of TNFα release and to functional antagonism towards 5-HT induced bronehoconstriction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1993.tb03240.x
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  • 4
    Electronic Resource
    Electronic Resource
    Fluticasone inhibits the progression of allergen-induced structural airway changes (2002)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 32 (2002), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Inhaled corticosteroids are widely used as first-line therapy in patients with asthma. The concept of early introduction is more and more accepted.Objective In our rat model of airway remodelling, we investigated whether treatment with inhaled fluticasone propionate can inhibit further progression of established structural airway changes.Methods Sensitized Brown Norway rats were exposed to aerosolized ovalbumin (1%) from day 14 to 42. From day 28 to 42, animals were treated with inhaled fluticasone or placebo 30 min before each allergen challenge. One control group was exposed to PBS from day 28 to 42, a second control group throughout the whole experiment.Results Exposure to ovalbumin during 2 weeks induced structural airway changes, including epithelial cell proliferation, increase in airway wall area and fibronectin deposition. Goblet cell number was increased, although not significantly compared with PBS. Continuing allergen exposure for 2 weeks further enhanced each of these features. In addition, the amount of collagen in the airway wall was enhanced by 4 weeks allergen exposure compared with PBS-exposed animals. These additional increases were inhibited by treatment with fluticasone during the last 2 weeks.Conclusion The progression of established allergen-induced structural airway changes in sensitized rats can be inhibited by treatment with fluticasone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2002.01394.x
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  • 5
    Electronic Resource
    Electronic Resource
    Differential effects of inhaled budesonide and oral prednisolone on serum immunoglobulin G and its subclasses in healthy adult volunteers (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Glucocorticosteroid (GCS) treatment lowers serum IgG and IgG subclass (IgG-SC) levels, but the minimal dose and duration of administration at which this occurs is not known.Objective The aim of this study was to define the daily dose of a 2-week course of GCS at which IgG(-SC) suppression occurs.Methods The effects of three GCS treatment schemes on serum IgG(-SC) levels in healthy adults were studied in a double-blind, randomized trial. Group I (n= 10) was treated with 40mg oral prednisolone/day, group 2 (n= 10) with 10 mg oral prednisolone/day and group 3 (n= 10) with 3.2 mg inhaled budesonide/day. Blood sampling was performed at baseline and at the end of the 2-week treatment period.Results In group 1, IgGl, IgG2 and lgG3 levels were significantly decreased after treatment, while in group 2 this was only so for IgG3. In both groups, the decrease of total IgG tended towards or just reached significance. In group 3, no statistically significant changes were observed.Conclusion A course of 40mg oral prednisolone/day for 2 weeks induces significant suppression of serum IgG-SC levels; lower doses cause more subtle changes, indicating that GCS-induced IgG-SC suppression is a dose-dependent phenomenon. Short courses of very high doses of inhaled budesonide appear to be devoid of this side-effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1997.tb00692.x
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  • 6
    Electronic Resource
    Electronic Resource
    Attenuation of allergic airway inflammation in IL-4 deficient mice (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 24 (1994), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To investigate the role of IL-4 in vivo in allergic asthma, we developed a murine model of allergen-induced airway inflammation. Repealed daily exposures of actively immunised C57BL/6 mice to aerosolized ovalbumin (OVA) induced a peribronchial inflammation and an increase in eosinophils and lymphocytes in bronchoalveolar-lavage(BAL) fluid. In IL-4 deficient (IL4−/−) mice, treated in the same way, there were substantially fewer eosinophils in BAL and much less peribronchial inflammation compared with wild type mice. In this model, mast cell deficient (W/Wv) mice developed a similar degree of BAL eosinophilia and peribronchial inflammation as wild type mice, demonstrating that the mast cell is not required for the induction of chronic airway inflammation. In contrast, BAL eosinophilia and airway inflammation were absent in OVA-treated MHC ClassII deficient (B6.Aa−/−) mice which lack mature CD4+ T lymphocytes. In conclusion, these results indicate that IL-4 is a central mediator of allergic airway inflammation, regulating antigen-induced eosinophil recruitment into the airways by a T cell dependent mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1994.tb00920.x
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  • 7
    Electronic Resource
    Electronic Resource
    The potential role of tumour necrosis factor a in asthma (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 23 (1993), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1993.tb00317.x
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  • 8
    Electronic Resource
    Electronic Resource
    Is Th1 the solution for Th2 in asthma? (2002)
    Oxford, UK : Blackwell Science, Ltd
    Clinical & experimental allergy 32 (2002), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0022-0477.2001.01279.x
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  • 9
    Electronic Resource
    Electronic Resource
    Report of an international workshop on risk and safety of asthma therapy (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 24 (1994), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1994.tb00214.x
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of ozone exposure on allergic sensitization and airway inflammation induced by dendritic cells (2002)
    Oxford, UK : Blackwell Science, Ltd
    Clinical & experimental allergy 32 (2002), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Epidemiological studies suggest that ozone exposure is related to increased asthma symptoms. Dendritic cells (DCs) are the principal antigen-presenting cells in the airways.Objective We have examined whether ambient doses of ozone (100 ppb for 2 h) enhance allergic sensitization and/or airway inflammation in a mouse model.Methods C57BL/6 mice were sensitized to inhaled ovalbumin (OVA) by intratracheal instillation of OVA-pulsed DCs on day 0. Daily exposure to OVA aerosol on days 14–20 resulted in an eosinophilic airway inflammation, as reflected in bronchoalveolar lavage fluid and lung histology. In a first experiment, mice were exposed to ozone or room air immediately prior to and following sensitization. Subsequently, we tested the effect of ozone exposure during antigen challenge in DC-sensitized mice.Results Exposure to ozone during sensitization did not influence airway inflammation after subsequent allergen challenge. In contrast, in sensitized mice, challenge with OVA together with ozone (days 14–20) resulted in enhanced airway eosinophilia and lymphocytosis, as compared with mice exposed to OVA and room air (1.91 × 106 ± 0.46 × 106 vs. 0.16 × 106 ± 0.06 × 106 eosinophils/mL lavage fluid; P = 0.015; 0.49 × 106 ± 0.11 × 106 vs. 0.08 × 106 ± 0.03 × 106 lymphocytes/mL lavage fluid; P = 0.004). Ozone exposure without subsequent OVA exposure did not cause airway inflammation.Conclusion Ozone exposure does not increase allergic sensitization but enhances antigen-induced airway inflammation in mice that are sensitized via the airways.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2002.01364.x
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