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Published on: January 21, 2018
Selective nasal allergen provocation induces substance P-mediated bronchial hyperresponsiveness
Greet Hens1, Ulrike Raap, Jeroen Vanoirbeek
1University Hospital Leuven, Division of Otorhinolaryngology, Kapucijnevoer 33, 3000 Leuven, Belgium.
Summary
Nasal allergen exposure triggers rapid bronchial hyperresponsiveness in mice by increasing substance P (SP) and activating neurokinin (NK) 1 receptors. This occurs even without inflammatory cell recruitment, highlighting a direct nasobronchial pathway.
Area of Science:
- Immunology
- Pulmonology
- Neuroscience
Background:
- The interaction between upper and lower airways in allergic conditions is not fully understood.
- Studying nasal allergen effects on lower airways is challenging due to allergen penetration.
- The concept of "global airway allergy" is increasingly recognized.
Purpose of the Study:
- To investigate the mechanisms of nasobronchial interaction in experimental airway allergy.
- To determine if nasal allergen provocation directly impacts lower airway function.
- To elucidate the role of substance P and neurokinin 1 receptors in this interaction.
Main Methods:
- Ovalbumin-sensitized mice underwent nasal allergen provocation after surgical separation of upper and lower airways via tracheotomy.
- Bronchial hyperresponsiveness to methacholine was assessed.
- Substance P (SP) concentrations and SP-positive nerve counts in the lungs were measured.
- The effect of a neurokinin (NK) 1 receptor antagonist was evaluated.
Main Results:
- Nasal allergen provocation induced rapid bronchial hyperresponsiveness within 4 hours, independent of inflammatory cell influx.
- Increased SP concentration in the bronchial lumen and elevated SP-positive pulmonary nerves were observed.
- Treatment with an NK1 receptor antagonist blocked allergen-induced bronchial hyperresponsiveness.
- Direct endobronchial administration of SP caused NK1 receptor-dependent bronchial hyperresponsiveness.
Conclusions:
- Nasal allergen provocation rapidly induces bronchial hyperresponsiveness through a mechanism involving pulmonary substance P (SP) up-regulation and neurokinin (NK) 1 receptor activation.
- This pathway mediates nasobronchial interaction in airway allergy.
- Targeting the SP/NK1 receptor pathway may offer therapeutic strategies for allergic airway diseases.
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