ATIONALE: 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.
Increased deposition of activated complement in peripheral lung vessels of smokers
CARAMORI, Gaetano;CASOLARI, Paolo;CONTOLI, Marco;PAPI, Alberto
2010
Abstract
ATIONALE: 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.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
