Rationale: In patients with chronic inflammatory lung disease pulmonary proteases can generate neoantigens from elastin and collagen with the potential to fuel autoreactive immune responses. Anti-elastin peptide antibodies have been implicated in the pathogenesis of tobacco-smoke induced emphysema. Collagen-derived peptides may also have a role. Objectives: We aimed to determine whether autoantibodies directed against elastin- and collagen-derived peptides are present in plasma from three groups of patients with chronic inflammatory lung disease compared to a non-smoking healthy control group, and to identify whether autoimmune responses to these peptides may be an important component of the disease process in these patients. Methods: 124 patients or healthy controls were recruited for the study (Z-A1AT deficiency, n=20; cystic fibrosis, n=40; chronic obstructive pulmonary disease, n=31; healthy control, n=33). C reactive protein, interleukin-32 and anti-nuclear antibodies were quantified. Anti-elastin and anti-N-Acetylated-proline-glycine-proline autoantibodies were measured by reverse ELISA. Measurements and Main Results: All patients were deemed stable and non-infective on the basis of absence of clinical or radiographic evidence of recent infection. There were no significant differences in levels of autoantibodies or IL-32 in the patients groups compared to the healthy controls. Conclusion: Anti-elastin or anti-N-Acetylated proline-glycine-proline autoantibodies are not evident in chronic inflammatory lung disease.