Nasal allergen provocation induces adhesion molecule expression and tissue eosinophilia in upper and lower airways
Open accessAbstract
Background Allergic rhinitis (AR) and asthma are characterized by means of a similar inflammatory process in which eosinophils are important effector cells. The migration of eosinophils from the blood into the tissues is dependent on adhesion molecules.Objective To analyze the aspects of nasobronchial cross-talk, we studied the expression of adhesion molecules in nasal and bronchial mucosa after nasal allergen provocation (NP).Methods Nine nonasthmatic subjects with seasonal AR and 9 healthy control subjects underwent NP out of season. Bronchial and nasal biopsy specimens were taken before (T(0)) and 24 hours after NP (T(24)). Mucosal sections were analyzed for the presence of eosinophils, IL-5, eotaxin, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and human endothelium (CD31).Results At T(24), an influx of eosinophils was detected in nasal epithelium (P =.01) and lamina propria (P <.01), as well as in bronchial epithelium (P =.05) and lamina propria (P <.05), of the patients with AR. At T(24), increased expression of ICAM-1, as well as increased percentages of ICAM-1+, VCAM-1+, and E-selectin+ vessels, were seen in nasal and bronchial tissue of patients with AR. The number of mucosal eosinophils correlated with the local expression of ICAM-1, E-selectin, and VCAM-1 in patients with AR.Conclusion This study shows that NP in patients with AR results in generalized airway inflammation through upregulation of adhesion molecules.
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The systemic allergic response is characterized by increased expression of adhesion molecules VCAM-1 and E-selectin on nasal and bronchial endothelium, facilitating migration of inflammatory cells into tissue.
“The systemic allergic response is further characterized by increased expression of adhesion molecules, such as vascular cell adhesion molecule 1 and E-selectin on nasal and bronchial endothelium, which facilitates the migration of inflammatory cells into the tissue.352”
From International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis (2018) · cites this paper as [352]
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- Authors
- Braunstahl, G.-J., Overbeek, S. E., KleinJan, A., Prins, J.-B., Hoogsteden, H. C., & Fokkens, W. J.
- Affiliations
- Erasmus MC (NL)
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2001-03
- Volume
- 107
- Issue
- 3
- Pages
- 469-476
- ISSN
- 0091-6749 (ISSN-L)
- OpenAlex
- W1964661356
- Cited by
- 454
- References
- 40
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 9 · 2023: 19 · 2022: 20 · 2021: 11 · 2020: 18 · 2019: 12 · 2018: 14 · 2017: 20 · 2016: 15 · 2015: 15 · 2014: 20 · 2013: 23 · 2012: 23
- FWCI
- 10.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Allergy and Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Funders
- Erasmus Universitair Medisch Centrum Rotterdam
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Immunology and Allergy › Food Allergy and Anaphylaxis Research
- Keywords
- allergic rhinitis, eosinophils, adhesion molecules, ICAM-1, VCAM-1, E-selectin, eosinophil migration, upper and lower airway inflammation, IL-5, eotaxin, bronchial mucosa, nasal mucosa
- MeSH terms
- Adult, Biopsy, Bronchi, Eosinophilia, Eosinophils, Female, Rhinitis, Allergic, Seasonal, Humans, Immunohistochemistry, Leukocyte Count, Male, Mucous Membrane, Nasal Mucosa, Nasal Provocation Tests, Pain Measurement, Biomarkers, Cell Adhesion Molecules, Interleukin-5, Inflammation Mediators, Vascular Cell Adhesion Molecule-1, E-Selectin
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