To the Editors:
Several studies indicate that an autoimmune response may underlie the pathogenesis of chronic obstructive pulmonary disease (COPD). A high prevalence of anti-Hep-2 epithelial cell autoantibodies has been shown in patients with COPD 1, 2, as well as autoantibodies against airway epithelial cells 1, endothelial cells 3, lung elastin 4, several immunogenic peptides 5 and cytokeratin 18 6. The most convincing evidence for an autoimmune response in COPD was provided by Lee et al. 4. They showed a specific autoantibody and a specific T-cell response against elastin in COPD patients, as well as increased numbers of anti-elastin antibody-producing cells in the lungs of COPD patients. Recent studies 7, 8, however, could not confirm such an anti-elastin autoantibody response. Cottin et al. 7 found no evidence for an anti-elastin autoantibody response in patients with combined pulmonary fibrosis and emphysema. Additionally, Greene et al. 8 investigated the presence of autoantibodies against elastin- and collagen-derived proline–glycine–proline in patients with COPD and α1-antitrypsin deficiency, and also did not observe increased autoantibody levels.
We assessed the presence of autoantibodies against elastin, collagen and decorin in serum of COPD patients and healthy controls. In addition, and as an extension of previous studies, we included equal numbers of current, ex- and never-smokers, in order to investigate the effect of the smoking status on autoantibody levels. We chose to asses autoantibodies against elastin and collagen to confirm the previous results of Lee et al. 4 in two different patient groups. As we previously demonstrated a decreased presence of the extracellular …