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Allergic inflammation and its pharmacological modulation in asthma
S T Holgate1, R Djukanović, J Wilson
1Immunopharmacology Group, Southampton General Hospital, UK.
International Archives of Allergy and Applied Immunology
|January 1, 1991
Summary
Asthma involves immediate and late reactions, with eosinophils and mast cells driving symptoms. Topical corticosteroids may work by inhibiting cytokines that regulate these inflammatory cells.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- Asthma pathogenesis involves atopy, but clinical expression is complex.
- Allergen exposure triggers immediate bronchoconstriction via mast cell mediators.
- Late asthmatic reactions involve eosinophils, leading to airway inflammation and hyperresponsiveness.
Purpose of the Study:
- To elucidate the cellular and molecular mechanisms underlying asthma.
- To understand the role of mast cells, eosinophils, and T lymphocytes in asthma.
- To identify potential therapeutic targets for asthma control.
Main Methods:
- Review of existing literature on asthma pathophysiology.
- Analysis of data from endobronchial biopsies and bronchoalveolar lavage.
- Investigation of cellular interactions and mediator functions in asthma.
Main Results:
- Both mast cells and eosinophils are key players in asthma-related airway dysfunction.
- T lymphocytes regulate mast cell and eosinophil activity.
- Cytokines, including interleukin-3, -4, and -5, are implicated in regulating these cells.
Conclusions:
- Asthma involves complex interactions between immune cells and inflammatory mediators.
- Targeting T-lymphocyte-controlled pathways, particularly cytokine regulation of mast cells and eosinophils, is a promising therapeutic strategy.
- Topical corticosteroids likely exert their effects by modulating these cellular and cytokine-driven processes.