The expression of HDAC2 is reported as reduced in
chronic obstructive pulmonary disease (
COPD). We assessed HDAC2 expression within the airways of smokers and subjects with
COPD and effects of inhaled
corticosteroids (ICS), using immuno-histology to contrast with previous molecular methodology. Endobronchial biopsies (ebb) from current smokers with
COPD (
COPD-CS; n = 15), ex-smokers with
COPD (
COPD-ES; n = 17), smokers with normal lung function (NS; n = 16) and normal controls (NC; n = 9) were immunostained for HDAC2. A double-blinded, randomized, placebo-controlled 6 months intervention study assessed effects of ICS on HDAC2 in 34
COPD subjects. There was no difference in epithelial HDAC2 staining in all groups. There was a significant reduction in total cell numbers in the lamina propria (LP) in
COPD-CS and NS (p<0.05). LP cellularity correlated inversely with smoking history in
COPD-CS (R = -0.8, p<0.003). HDAC2 expression increased markedly in NS (p<0.001); in contrast
COPD-CS was associated with suppressed signal (p<0.03), while normal in
COPD-ES. ICS did not affect HDAC2 cell staining. Our findings suggest that airway HDAC2 expression is increased in the LP by smoking itself, but is reduced in
COPD. Ex-smokers have normalised HDAC2 cell expression, but ICS had no effect. The paper emphasise the pit-falls of relying on molecular data alone to define airway changes.
CLINICAL TRIAL REGISTRATION INFORMATION: The Australian New Zealand Clinical Trials Registry (ANZCTR). REGISTRY NUMBER: ACTRN12612001111864.