Increased deposition of activated complement in peripheral lung vessels of smokers

RATIONALE: Previous studies suggest that an autoimmune response, mediated by autoantibodies directed against lung epitopes, may contribute to the pathogenesis of severe chronic obstructive pulmonary disease (COPD). A cardinal feature of antibody-mediated rejection in renal allografts includes evidence for antibody action, such as complement (C) activation demonstrated by C4d deposition. AIM AND METHODS: The aim of our study was to investigate by immunohistochemistry (IHC), using the appropriate positive and negative controls, the expression of the complement C4d subunit in formalin-fixed paraffin-embedded peripheral lung, obtained during lung resection surgery, from 14 age-matched non-smokers subjects, 20 smokers with normal lung function and 17 smokers with COPD. RESULTS: The IHC staining was mainly confined to lung vessels and the number of C4d+ve lung vessels was significantly increased in smokers (with or without COPD) compared to non-smokers. CONCLUSION: These data suggest that an autoantibody-mediated immune response, although enhanced by smoking, may not be critical for causing the peripheral lung damage seen in the COPD patients.