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Published on: April 14, 2010
Anti-inflammatory agents and allergen-induced beta2-receptor dysfunction in isolated human bronchi
1Centro di Fisiopatologia Respiratoria, Dipartimento di Scienze Motorie e Riabilitative, Università di Genova, Genova, Italy.
Antigen challenge impairs beta2-adrenoceptor function in human airways. Nedocromil sodium and iralukast protected against this dysfunction, suggesting leukotrienes contribute to airway hyperresponsiveness.
Area of Science:
- Respiratory Medicine
- Pharmacology
- Immunology
Background:
- Antigen exposure can lead to beta2-adrenoceptor dysfunction in sensitized human bronchi.
- The potential for anti-inflammatory agents to prevent this dysfunction requires investigation.
Purpose of the Study:
- To determine if anti-inflammatory drugs can prevent antigen-induced beta2-adrenoceptor dysfunction in human bronchi.
- To explore the role of peptido-leukotrienes in this allergic airway response.
Main Methods:
- Human bronchial rings were passively sensitized to house dust mite.
- Rings were challenged with allergen alone or with allergen plus indomethacin, nedocromil sodium, cetirizine, or iralukast.
- Beta2-adrenoceptor function was assessed by measuring salbutamol-induced relaxation after carbachol contraction.
Main Results:
- Allergen challenge alone significantly impaired salbutamol-induced relaxation, indicating beta2-adrenoceptor dysfunction.
- Nedocromil sodium and iralukast (at higher concentrations) significantly improved salbutamol-induced relaxation.
- Cetirizine and indomethacin did not significantly alter the response compared to allergen alone.
Conclusions:
- Peptido-leukotriene release appears to play a significant role in allergen-induced beta2-adrenoceptor dysfunction.
- Nedocromil sodium and iralukast demonstrate protective effects against this dysfunction.
- These findings suggest potential therapeutic targets for managing allergic airway inflammation.
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