RT Journal Article
SR Electronic
T1 Lung function decline in COPD in relation to MMP-12 and surfactant protein A
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP PA4008
DO 10.1183/13993003.congress-2016.PA4008
VO 48
IS suppl 60
A1 Annelie Behndig
A1 Robert Linder
A1 Jamshid Pourazar
A1 Anne Lindberg
A1 Anders Blomberg
YR 2016
UL http://erj.ersjournals.com/content/48/suppl_60/PA4008.abstract
AB Rationale:Matrix metalloproteinases (MMPs) are of significance in the pathogenesis of COPD. Surfactant proteins (SPs) are involved in immunity and important in the airway defence against infectious agents. We hypothesized that the airway levels of MMPs and SPs would be modified in COPD, in relations to healthy non-smoking individuals, and that COPD patients with more rapid lung function decline would be even further affected.Methods: 22 patients with COPD were recruited from a population-based cohort (OLIN), (9 with stable lung function (LF), 13 with rapid LF decline; mean yearly FEV1 decline <30 ml and >60 ml respectively), along with 15 smokers and 15 never-smokers with normal LF. Bronchoscopy with bronchial wash (BW 2x20 ml), bronchoalveolar lavage (BAL 3x60 ml) was performed, with quantification of MMP-9, MMP-12, TIMP-1 and Sp-A.Results: BW and BAL concentrations of MMP-12 were increased in COPD compared with never-smokers; p=0.005 and p=0.005 respectively. In contrast, levels of SP-A were clearly decreased in COPD compared with the control groups; p<0.001 and p<0.001. When comparing responses between COPD-cases with rapid LF decline and stable disease, MMP-12 concentrations were higher in rapid decliners compared to subjects with stable disease. BW and BAL TIMP-1-levels were higher in COPD compared with never-smokers; p=0.008 and p=0.001 respectively.Conclusions: This study shows evidences of an increased proteolytic activity along with a decreased infectious defence in the COPD airways. As MMP-12 is one of the major proteolytic enzymes to induce airway remodelling in COPD, MMP-12-related lung tissue destruction may be one important mechanism behind rapid lung function loss in COPD.