To our knowledge, the expression and activity of 11β-HSD has not been determined in patients with severe asthma or COPD, where Tonello and Poli correctly state that oxidative stress is high. The ability of GCs to increase 11β-HSD expression under the control of CCAAT/enhancer-binding protein (C/EBP) β has been previously shown.5 Primary human epithelial cells elicit an acute-phase response following stimulation, and GCs can spare the expression of host defense molecules, including complements, collectins, and other antimicrobial proteins. In that study by Zhang et al,5 the knockdown of C/EBPβ blocked the induction of host defense molecules by GC but had no effect on inflammatory gene expression. The expression of C/EBPα, but not C/EBPβ, is markedly reduced in airway smooth muscle of asthmatic patients,6 and in culture budesonide enhanced C/EBPβ expression.7 In contrast, the expression of C/EBPα and C/EBPβ was unaltered in COPD patients but was attenuated by budesonide.7 However, the expression of C/EBP isoforms is not known in patients with severe asthma. Since there is disease-specific expression and regulation of C/EBP isoforms, there remains a possibility that pharmacologic manipulation of 11β-HSD activity might act to enhance the activity of endogenous GCs and thereby overcome GC resistance, particularly in relation to the induction of innate immune mediators.