However, the Childhood Asthma Management Program study reported no significant long-term prevention in the decline of lung function with ICS in children presenting mild-to-moderate asthma. Whether the decline in lung function is preventable in asthma needs to be confirmed. ICS has no effect on FEV1 decline, respiratory symptoms and exacerbations in mild to moderate COPD, while in moderate to severe COPD, a positive effect is seen. This reflects the facts that inflammation in COPD is different from asthma-associated inflammation and that damages are mostly irreversible. In CF, oral corticosteroids appear to slow the progression of the disease. review
Effect of Corticosteroids on Inflammation: ICS are the mainstay of asthma therapy and are currently the most effective way to control inflammation, particularly of the eosinophilic type. Reduced number of airway mast cells, eosinophils, CD4+ T-cells, and CD8+ T cells by either ICS or oral corticosteroids is well documented in asthma disease. Oral corticosteroids or ICS also decrease the messenger RNA expression of GM-CSF, IL-4, IL-5, and increase mterferon-7.
Therefore, ICS could possibly influence remodeling through their antiinflammatory effects. However, ICS are much less effective in reversing airway remodeling than inflammation. Oral corticosteroids significantly reduced the expression of two profibrotic cytokines, IL-17 and IL-11, in patients with moderate-to-severe asthma but interestingly had no effect on TGF-^ expression. In RADS, despite corticosteroid treatment, recovery is often incomplete with persistence of inflammation and airway fibrosis.
The effects of ICS on airway inflammation have been studied on COPD and are disappointing. No reduction in CD8+ T-cells, CD68+ cells, or neutrophils is seen after ICS treatment. Decreased CD8:CD4 ratio in the epithelium, increased neutrophils, and reduced number of mast cells in the subepithelial area following three months of ICS treatment were found in COPD endobronchial bi-opsies.