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Nasal challenge studies with bradykinin: influence upon mediator generation
1Department of Clinical Immunology and Asthma Policlinic, Free University, Berlin, Germany.
Summary
Intranasal bradykinin (Bk) causes dose-dependent plasma leakage in the nasal cavity, especially in allergic rhinitis patients. This suggests kinins are key mediators in upper airway inflammation.
Area of Science:
- Immunology
- Otorhinolaryngology
- Pharmacology
Background:
- Nasal allergen exposure increases inflammatory mediators like histamine and kinins.
- Understanding the interaction of these mediators is crucial for rhinitis research.
Purpose of the Study:
- To investigate the effects of intranasal bradykinin (Bk) on nasal lavage mediators and symptoms.
- To determine if Bk influences plasma leakage and mast cell mediators in allergic rhinitis patients.
Main Methods:
- Eight grass-pollen-allergic patients and five controls received escalating doses of intranasal Bk.
- Nasal lavages were analyzed for albumin, TAME esterase activity, histamine, LTC4, and PGD2 metabolite (9α,11β-PGF2).
- Clinical symptoms were recorded using a subjective score.
Main Results:
- Bk induced a dose-dependent increase in nasal albumin, indicating plasma leakage, significantly higher in rhinitis patients.
- TAME esterase activity also increased with Bk dosage, with no significant group differences.
- Histamine, LTC4, and 9α,11β-PGF2 levels remained unchanged, suggesting no mast cell degranulation.
Conclusions:
- Intranasal Bk causes dose-dependent plasma leakage in the nasal cavity, more pronounced in allergic rhinitis patients.
- Bk does not appear to activate mast cells, as key mediators were not released.
- Kinins are likely important mediators in upper airway inflammatory disorders, contributing to rhinitis symptoms.