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Cytokines and adhesion molecules in allergic rhinitis
C Bachert1, M Wagenmann, G Holtappels
1ENT Department, University Hospital Düsseldorf, Germany.
American Journal of Rhinology
|March 26, 1998
Summary
Allergic rhinitis involves nasal inflammation with increased immune cells like eosinophils. While allergen exposure triggers mediator release, the exact mechanisms of cell recruitment, especially eosinophils, and the role of chemokines require further investigation.
Area of Science:
- Immunology
- Allergy Research
- Rhinology
Background:
- Allergic rhinitis is characterized by nasal inflammation.
- Immune cell infiltration, including eosinophils, basophils, and mast cells, occurs upon allergen exposure.
- Existing knowledge on allergic inflammation relies on studies of cytokines, chemokines, and adhesion molecules.
Purpose of the Study:
- To review current knowledge of nasal allergic inflammation.
- To explore the roles of cytokines, chemokines, and adhesion molecules in allergic rhinitis.
- To discuss aspects of viral rhinitis in comparison.
Main Methods:
- Review of existing literature on allergic rhinitis.
- Analysis of studies focusing on cytokines, chemokines, and adhesion molecules.
- Examination of immune cell responses to allergen exposure.
Main Results:
- Allergen exposure leads to increased eosinophils, basophils, mast cells, IgE-positive cells, macrophages, and T-cells in nasal mucosa.
- Proinflammatory and regulatory cytokines are released after antigen challenge, with TH2-type cytokine mRNA upregulation observed.
- Proinflammatory cytokines initiate adhesion cascades and T-cell activation, potentially influencing long-term eosinophil recruitment.
Conclusions:
- Allergic rhinitis is an inflammatory condition.
- The precise mechanisms for acute eosinophil migration post-allergen challenge are not fully elucidated.
- The roles of chemokines in both allergic and viral rhinitis warrant further research.