Human β-
defensin 2 (hBD-2) has antimicrobial activity and may play a role in airway mucosal defense, but studies have not yet examined its expression in lung tissue of patients with
chronic obstructive pulmonary disease (
COPD). Here we investigated hBD-2 levels in lung tissues of
COPD patients and analyzed their correlations with
IL-8, IL-1β, cigarette smoking and lung function in order to see whether the
protein may be involved in pathogenesis of the disease. Peripheral lung tissue specimens were obtained from 51 patients who underwent lung resection for peripheral
lung cancer: healthy non-smokers (n=8), healthy current smokers (n=7), non-smokers with
COPD (n=11), and current smokers with
COPD (n=25). RT-PCR and immunohistochemical staining were used to detect expression levels of hBD-2,
IL-8 and IL-1β. Expression of hBD-2
mRNA was significantly higher in
COPD patients than in healthy controls, and significantly higher in current smokers than in non-smokers (p<0.05). Among healthy controls, hBD-2
mRNA levels were similar between current smokers and non-smokers. Immunohistochemistry showed hBD-2
protein to be expressed mainly in epithelia of distal bronchioles and its expression pattern among our patient groups mirrored that of the
mRNA.
IL-8 mRNA levels were significantly higher in
COPD patients than in healthy controls (p<0.05), while IL-1β
mRNA levels did not differ significantly among the groups. Levels of hBD-2
mRNA positively correlated with levels of
IL-8 mRNA (r=0.545, p=0.002), and negatively correlated with FEV1/FVC ratios and with predicted FEV1% values (r=-0.406, p=0.011). Our results indicate that hBD-2 expression is elevated in distal airways of
COPD patients and that it may be involved in pathogenesis of the disease. Our data implicate cigarette smoking as
a factor that may elevate hBD-2 levels in lung tissues of
COPD patients.