Abstract
Asthma is the result of the interaction of genetic and environmental factors. Increased expression of inflammatory genes defines cellular and structural alterations on the respiratory system while environmental exposures modulate the different asthma phenotypes. Specific ambiental exposures and infections over a predisposed set of genes lead to a systemic propensity for allergic T helper type 2 (Th2) cell cytokine responses. This, associated to local immune events, generates an allergic airways inflammation. The interaction between local immune network andresident airway cell populations, key producers of cytokines, chemokines and growth factors, produces a chronic inflammatory respiratory disease, called asthma. In this scenario, inhaled steroids are considered the cornerstone in the management of chronic persistent asthma. Corticosteroids suppress the chronic inflammation in patients with asthma by reversing histone acetylation of the activated inflammatory genes. As the molecular mechanisms of action of corticosteroids are being elucidated, new information on asthma pathogenesis is becoming available and helping to shape asthma management.
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