Glucocorticoid
activities in the lung cells are summarised in Figure
3.
Figure 3: Cellular effects of corticosteroids.
Glucocorticoids affect both inflammatory and structural cells, leading to the suppression of chronic inflammation underlying asthma
development. In particular, this is due to a noteworthy reduction
of the number of eosinophils, T-lymphocytes, mast cells and macrophages, but also
to the effects on epithelial cells (decreased release of proinflammatory cytokines
and mediators) and endothelial cells (leak reduction) and also to a
reduced mucus secretion. This broad spectrum of effects of glucocorticosteroids
on bronchial inflammation in asthma leads to clinical improvements in asthma symptoms
and lung function, relevant reduction in airways hyperresponsiveness
and prevention of asthmatic exacerbations.4
Although ICSs are highly effective in asthma, they
provide little therapeutic benefit in COPD, when administered in monotherapy,
mainly because ICS minimally influence the specific inflammatory process
of COPD. In addition, there is increasing evidence for an active steroid resistance
in COPD, as corticosteroids fail to inhibit cytokines that they normally suppress,
like IL-8 and TNF-α.5 |
