Anti-proline-glycine-proline or antielastin autoantibodies are not evident in chronic inflammatory lung disease.
Greene, Catherine M Low, Teck Boon O'Neill, Shane J McElvaney, Noel G
Greene, Catherine M
Low, Teck Boon
O'Neill, Shane J
McElvaney, Noel G
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Advisors
Editors
Other Contributors
Date
2010-01-01
Date Submitted
Keywords
Other Subjects
Subject Mesh
Adolescent
Adult
Aged
Autoantibodies
Autoimmune Diseases
Case-Control Studies
Cystic Fibrosis
Elastin
Female
Humans
Male
Middle Aged
Oligopeptides
Pulmonary Disease, Chronic Obstructive
Smoking
Young Adult
alpha 1-Antitrypsin Deficiency
Adult
Aged
Autoantibodies
Autoimmune Diseases
Case-Control Studies
Cystic Fibrosis
Elastin
Female
Humans
Male
Middle Aged
Oligopeptides
Pulmonary Disease, Chronic Obstructive
Smoking
Young Adult
alpha 1-Antitrypsin Deficiency
Planned Date
Start Date
Collaborators
Principal Investigators
Alternative Titles
Publisher
Abstract
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.
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.
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.
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.
Antielastin or anti-N-acetylated proline-glycine-proline autoantibodies are not evident in chronic inflammatory lung disease.
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.
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.
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.
Antielastin or anti-N-acetylated proline-glycine-proline autoantibodies are not evident in chronic inflammatory lung disease.
Language
en
ISSN
1535-4970
eISSN
ISBN
DOI
10.1164/rccm.200904-0545OC
PMID
19762563