Background: Eosinophilic inflammation plays a central role in the pathogenesis of asthma. Striking inflammatory changes are present in the airways of patients with all levels of disease severity. The degree of airway inflammation correlates with airway hyperresponsiveness, the primary physiologic abnormality of asthma. Inflammation is typically initiated by immunologic events (including allergy) and is driven by mediators released by various cells of the immune system, particularly eosinophils, monocytes and macrophages, lymphocytes, and mast cells. Methods: Literature on asthma and the inflammatory response was drawn from recent articles presented and reviewed in journal clubs and from selected articles from the National Library of Medicine. Results and Conclusions: The inflammatory process can be divided into six steps: triggering, signaling, migration, inflammatory cell activation, tissue damage, and resolution. Recognition of the importance of inflammation in the pathogenesis of asthma and the progression of the disease has shifted research efforts and the development of new therapeutic agents toward reduction of airway inflammation. Anti-inflammatory therapy, which can be directed against specific steps in the inflammatory process, actually reduces bronchial hyperresponsiveness. Although anti-inflammatory management has assumed a primary role in asthma therapy, short acting β2-adrenergic receptor agonists are needed for treatment of acute symptoms, and some patients require regular β2-agonist therapy despite apparently adequate anti-inflammatory therapy.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of the American Board of Family Practice|
|State||Published - Nov 27 1996|
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health