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Pathophysiology of mild-moderate asthma

The advent of the fibreoptic bronchoscope has enable direct access to the lower airways of patients with asthma. Even in mild disease there is evidence of a vigorous inflammatory response characterised by mast cell activation and eosinophil infiltration, whose mediators cause the airway dysfunction characteristic of the disease. Both mast cells and eosinophils are under the control of a specific subpopulation of T-lymphocytes (TH2) through the release of cytokines, specifically IL-3, IL-4, IL-5, and GM-CSF. By uperegulating endothelial leukocyte adhesion molecules (specifically ELAM-1, ICAM-1, and UCAM-1) leukocytes are entrapped within the bronchial vasculature and, under the influence of chemoattractants, migrate into the airway wall. In addition to causing smooth muscle contraction and microvascular leakage, mast cell and eosinophil dependent mediators break down the intercellular adhesion proteins of the overlying epithelium, thereby breaking the permeability barrier and exposing afferent nerve endings. In response to this there is proliferation of myofibroblasts that not only alter the mechanical properties of the airway through excess collagen deposition, but also provide a source for additional multifactorail cytokines. From the observations it is clear that treatment of asthma should be more directed towards prevention and use of agents that reduce the inflammatory response rather than the current practice of relying upon bronchodilators to relieve symptoms[1, 2].

References

1. Holgate, S.T.: Pathophysiology of Mild-Moderate Asthma. In Asthma

from theory to practice. Fisons Symposium in Congress of EAACI, Paris, May 12, 1992.

2. Oddera S, Silvestri M, Balbo A, Jovovich BO, Penna R, Crimi E, Rossi GA. Airway eosinophilic inflammation, epithelial damage, and bronchial hyperresponsiveness in patients with mild-moderate, stable asthma. Allergy. 1996 Feb;51(2):100-7.