The anti-inflammatory effect of glucocorticoids is mediated by glucocorticoid-induced leucine zipper in epithelial cells.

Background: Nuclear factor kappaB (NF-kappaB) plays a key role in the pathogenesis of asthma, being linked to the production of inflammatory cytokines that drive inflammation. A recently described anti-inflammatory protein, glucocorticoid-induced leucine zipper (GILZ), interferes with NF-kappaB-mediated gene transcription in T cells and macrophages.

Objective: We sought to analyze the regulation of GILZ expression in airway epithelial cells and determine whether GILZ mediates part of the anti-inflammatory effect of corticosteroids.

Biologic therapies for the treatment of asthma.

Asthma is a chronic disease of the airway whose pathogenesis involves the complex interplay between many cell types and inflammatory mediators. The mainstays of therapy, inhaled bronchodilators and corticosteroids, do not target the asthmatic airway specifically and therefore are associated with untoward side effects. Anti-IgE (omalizumab) is the only biologic therapy to have transitioned completely from bench to bedside.