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

Hdl Handle:
http://hdl.handle.net/10147/127274
Title:
Anti-proline-glycine-proline or antielastin autoantibodies are not evident in chronic inflammatory lung disease.
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
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
Issue Date:
1-Jan-2010
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
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
ISSN:
1535-4970

Full metadata record

DC FieldValue Language
dc.contributor.authorGreene, Catherine Men
dc.contributor.authorLow, Teck Boonen
dc.contributor.authorO'Neill, Shane Jen
dc.contributor.authorMcElvaney, Noel Gen
dc.date.accessioned2011-04-05T15:37:18Z-
dc.date.available2011-04-05T15:37:18Z-
dc.date.issued2010-01-01-
dc.identifier.citationAnti-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.en
dc.identifier.issn1535-4970-
dc.identifier.pmid19762563-
dc.identifier.doi10.1164/rccm.200904-0545OC-
dc.identifier.urihttp://hdl.handle.net/10147/127274-
dc.description.abstractIn 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.-
dc.description.abstractTo 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.-
dc.description.abstractA 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.-
dc.description.abstractAll 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.-
dc.description.abstractAntielastin or anti-N-acetylated proline-glycine-proline autoantibodies are not evident in chronic inflammatory lung disease.-
dc.language.isoenen
dc.relation.urlhttp://ajrccm.atsjournals.org/cgi/reprint/181/1/31en
dc.subject.meshAdolescent-
dc.subject.meshAdult-
dc.subject.meshAged-
dc.subject.meshAutoantibodies-
dc.subject.meshAutoimmune Diseases-
dc.subject.meshCase-Control Studies-
dc.subject.meshCystic Fibrosis-
dc.subject.meshElastin-
dc.subject.meshFemale-
dc.subject.meshHumans-
dc.subject.meshMale-
dc.subject.meshMiddle Aged-
dc.subject.meshOligopeptides-
dc.subject.meshPulmonary Disease, Chronic Obstructive-
dc.subject.meshSmoking-
dc.subject.meshYoung Adult-
dc.subject.meshalpha 1-Antitrypsin Deficiency-
dc.titleAnti-proline-glycine-proline or antielastin autoantibodies are not evident in chronic inflammatory lung disease.en
dc.typeArticleen
dc.contributor.departmentDepartment of Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin, Ireland. cmgreene@rcsi.ieen
dc.identifier.journalAmerican journal of respiratory and critical care medicineen
dc.description.provinceLeinster-

Related articles on PubMed

All Items in Lenus, The Irish Health Repository are protected by copyright, with all rights reserved, unless otherwise indicated.