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The pathobiology of bronchial asthma
1Department of Allergy and Allied Respiratory Disorders, U.M.D.S., Guy's Hospital, London, England.
Advances in Immunology
|January 1, 1992
Summary
Asthma involves significant airway inflammation, characterized by cellular infiltration and mediator release. Research highlights the crucial role of cytokines like IL-5 and GM-CSF in eosinophil function and disease severity.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- Early studies indicated significant bronchial inflammation in fatal asthma cases.
- Histological and lavage studies confirm airway inflammation in mild asthma, including epithelial changes and inflammatory cell infiltration.
Purpose of the Study:
- To investigate the cellular and molecular mechanisms underlying airway inflammation in asthma.
- To explore the role of cytokines and adhesion molecules in asthma pathogenesis.
Main Methods:
- Histological examination of bronchial biopsies.
- Analysis of bronchoalveolar lavage fluid.
- In situ hybridization to detect cytokine mRNA.
- Characterization of cell adhesion molecules.
Main Results:
- Asthma airways show epithelial edema, collagen deposition, and infiltration of eosinophils, T lymphocytes, and macrophages.
- Increased expression of HLA class II molecules on airway cells.
- Elevated levels of cytokines like IL-3, IL-5, and GM-CSF, influencing eosinophil survival and function.
- Up-regulation of endothelial adhesion molecules (ELAM-1, ICAM-1) implicated in leukocyte recruitment.
Conclusions:
- Airway inflammation is central to asthma pathophysiology, with severity correlating to inflammatory markers.
- Cytokines and cell adhesion molecules play critical roles in the development and maintenance of asthma inflammation.
- Further research into these mechanisms can inform therapeutic strategies for asthma.
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