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Anti–Proline-Glycine-Proline or Antielastin Autoantibodies Are Not Evident in Chronic Inflammatory Lung Disease

¹ Respiratory Research Division, Department of Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin, Ireland

Correspondence and requests for reprints should be addressed to Catherine Greene, B.A., Ph.D., Respiratory Research Division, Department of Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland. E-mail: cmgreene{at}rcsi.ie

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. Antielastin peptide antibodies have been implicated in the pathogenesis of tobacco-smoke–induced emphysema. Collagen-derived peptides may also play a role.

Objectives: 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 with a nonsmoking 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: A total of 124 patients or healthy control subjects 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, IL-32, and antinuclear antibodies were quantified. Antielastin and anti–N-acetylated-proline-glycine-proline autoantibodies were measured by reverse ELISA.

Measurements and Main Results: All patients were deemed stable and noninfective on the basis of the absence of clinical or radiographic evidence of recent infection. There were no significant differences in the levels of autoantibodies or IL-32 in the patients groups compared with the healthy control subjects.

Conclusions: Antielastin or anti–N-acetylated proline-glycine-proline autoantibodies are not evident in chronic inflammatory lung disease.

Key Words: autoimmunity • IL-32 • -1 antitrypsin deficiency • cystic fibrosis • chronic obstructive pulmonary disease

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Autoimmune responses to elastin- and collagen peptides may have a role in the pathogenesis of tobacco-smoke-induced emphysema. What This Study Adds to the Field We demonstrate no evidence for systemic autoantibodies directed against elastin peptides or N-acetylated-proline-glycine-proline in chronic inflammatory lung disease.

 

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