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    Anti-proline-glycine-proline or antielastin autoantibodies are not evident in chronic inflammatory lung disease.

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    Authors
    Greene, Catherine M
    Low, Teck Boon
    O'Neill, Shane J
    McElvaney, Noel G
    Affiliation
    Department of Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin, Ireland. cmgreene@rcsi.ie
    Issue Date
    2010-01-01
    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
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    Citation
    Anti-proline-glycine-proline or antielastin autoantibodies are not evident in chronic inflammatory lung disease. 2010, 181 (1):31-5 Am. J. Respir. Crit. Care Med.
    Journal
    American journal of respiratory and critical care medicine
    URI
    http://hdl.handle.net/10147/127274
    DOI
    10.1164/rccm.200904-0545OC
    PubMed ID
    19762563
    Additional Links
    http://ajrccm.atsjournals.org/cgi/reprint/181/1/31
    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.
    Item Type
    Article
    Language
    en
    ISSN
    1535-4970
    ae974a485f413a2113503eed53cd6c53
    10.1164/rccm.200904-0545OC
    Scopus Count
    Collections
    Beaumont Hospital

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