European Respiratory Society


Liberation of elastin peptides from damaged lung may be a mechanism of autoimmune lung disease. Citrullination, and anti-citrullinated protein antibody formation occurs in smokers, but the role of smoking in autoantibody generation relevant to pulmonary disease is unclear.

Anti-elastin, anti CCP and anti-MCV antibodies were measured in 257 subjects with alpha 1 antitrypsin deficiency (AATD) , 113 subjects with usual COPD and 22 healthy non-smokers. Levels were compared between groups, against phenotypic features, and against smoke exposure.

Anti-elastin antibodies were higher in controls relative to AATD (p=0.008) and usual COPD (p<1×10−5), and in AATD relative to usual COPD (p<1×10−5). Anti-elastin levels showed a threshold at 10 pack years, being higher in those who had smoked less (p=0.004). No relationships between antibody levels and clinical phenotype were seen after adjustment for smoke exposure. Anti-CCP antibodies were higher in usual COPD than AATD (p=0.002) but the relationship to smoke exposure was less clear.

Smoke exposure is the main determinant of anti-elastin antibody levels, which fall after 10 pack years. Local antibody complexes may be a better measure of elastin directed autoimmunity than circulating levels.