ABSTRACT
Airway inflammation and immune activation play a key role in the pathogenesis of chronic asthma. Current guidelines of asthma therapy have therefore focused on the use of anti-inflammatory therapy, particularly inhaled glucocorticoids (GCs). The clinical efficacy of GCs are thought to result from a combination of effects on lung inflammation, including decreased trafficking of inflammatory cells to the lung; reduced inflammatory cell survival; diminished production of airway mucus; an inhibitory effect on inflammatory cytokine production; and other anti-inflammatory mechanisms, including the increased gene transcription of anti-inflammatory proteins (see Chapter 8 and Refs. 1,2). Asthmatics, however, vary in their responses to GCs. While the majority of patients respond to regular inhaled GC therapy, there are patients who respond poorly even when treated with high doses of oral prednisone (reviewed in Ref. 1). These patients are often referred to as ``steroid-resistant'' (SR) asthmatics and are distinguished
from ``steroid-sensitive'' (SS) patients, who respond rapidly to oral corticosteroids.
