In COPD, it was reported that high doses of ICS had no effect on sputum inflammatory cell number, IL-8 levels, elastase activity, MMP-1, MMP-9, SLPI, or TIMP-1. Systemic corticosteroids are used in a short-course pattern in exacerbated COPD, improving lung function and clinical outcomes. However, the antiinflammatory effect of such a short course of systemic corticosteroid treatment has not been addressed in COPD patients. As CD4+ T-cells and mast cells have not been linked to COPD inflammation, there are no convincing data on the potential therapeutic role of corticosteroids in COPD with the exception of exacerbated COPD and COPD with increased eosino-phils. In CF, ICS failed to reduce airway inflammation. In bronchiectasis, corticosteroids decreased T-cell infiltration and IL-8 levels, but clinical benefits are still not clear. more
Effect of Corticosteroids on Structural Cells: Corticosteroids have been reported to induce apoptosis in airway epithelial cells. Corticosteroids also reduced IL-6 cytokine production but not TNF-a-mediated increases in IL-8 or GM-CSF secretion in cultured epithelial cells. This might explain why corticosteroids fail to control neutrophilic inflammation in airway diseases. In another study, corticosteroids decreased chemokine production including growth-related oncogene-a and IL-8 by bronchial epithelial cells. From a clinical perspective, ICS were found to decrease mucus production in asthmatic patients. From the various models studied, the effect of corticosteroids on epithelial cells is still controversial, but they may be beneficial through a decrease in mucus production.
The effect of corticosteroids on fibroblasts has been poorly studied. Cultured nasal fibroblasts stimulated with bFGF or TNF-a have reduced proliferation rate and intracellular adhesion molecule-1 expression when treated with fluticasone. In the same way, bFGF-induced proliferation and DNA synthesis or TNF-a-induced intracellular adhesion molecule-1, monocyte chemotactic protein-1, eotaxin, and IL-6 release in human fetal lung fibroblasts can be reduced by corticosteroids. In an in vitro study, dexamethasone increased 3H-thymi-dine incorporation (promoting their proliferation) in asthmatic bronchial fibroblasts without having any significant effect on normal fibroblast proliferation.