dc.contributor.author | Quirke, A-M | |
dc.contributor.author | Perry, E | |
dc.contributor.author | Cartwright, A | |
dc.contributor.author | Kelly, C | |
dc.contributor.author | De Soyza, A | |
dc.contributor.author | Eggleton, P | |
dc.contributor.author | Hutchinson, D | |
dc.contributor.author | Venables, PJ | |
dc.date.accessioned | 2015-09-14T08:21:30Z | |
dc.date.issued | 2015-08-26 | |
dc.description.abstract | Objective: Bronchiectasis (BR) is a risk factor for rheumatoid arthritis (RA). Here we examine the potential of BR in generating rheumatoid factors (RFs) and anti-citrullinated peptide antibodies (ACPA) in patients with BR alone and in patients with BR and RA (BRRA). Methods: We studied 122 patients with BR alone, 50 BRRA, 50 RA without lung disease, with 87 asthma and 79 healthy subjects as controls. RFs were measured by an automated analyzer, and ACPA using CCP2. Fine specificities to citrullinated α-enolase (CEP-1), citrullinated vimentin (cVim) and fibrinogen (cFib) with their arginine control peptides (REP-1, Vim and Fib) measured by ELISA. Results: In the BR patients 39% were ever smokers compared to 42% of the controls. Serum samples from BR patients had an increased frequency of RF (25%; p< 0.05) and 5% to CCP2, 7% to CEP-1, 7% to cVIM (all p=ns) and 12% cFib (p <0.05). There was also a corresponding increase in antibodies to the arginine-containing control peptides in the BR patients; REP-1, 19% (p< 0.01) and Vim, 16% (p<0.05), demonstrating that the ACPA response in BR is not citrulline-specific. Lack of citrulline specificity was further confirmed by absorption studies. In BRRA all ACPA specificities were highly citrulline-specific. Conclusion: Bronchiectasis is an unusual but potent model for the induction of autoimmunity in RA by bacterial infection in the lung. Our study suggests that in the early stages of tolerance breakdown, the ACPA response is not citrulline-specific, but becomes more so in those patients with BR that develop BRRA. | en_GB |
dc.description.sponsorship | Arthritis Research UK | en_GB |
dc.description.sponsorship | European Union | en_GB |
dc.description.sponsorship | IMI project BTCure | en_GB |
dc.description.sponsorship | 7th Framework Programme project Gums and Joints | en_GB |
dc.identifier.citation | Vol. 67, No. 9, pp. 2335–2342 | en_GB |
dc.identifier.doi | 10.1002/art.39226 | |
dc.identifier.grantnumber | 19894 | en_GB |
dc.identifier.grantnumber | 115142-2 | en_GB |
dc.identifier.grantnumber | HEALTH-F2-2010-261460 | en_GB |
dc.identifier.uri | http://hdl.handle.net/10871/18226 | |
dc.language.iso | en | en_GB |
dc.publisher | Wiley | en_GB |
dc.relation.url | http://onlinelibrary.wiley.com/doi/10.1002/art.39226/abstract | en_GB |
dc.rights | This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. | en_GB |
dc.title.alternative | Bronchiectasis: a model for chronic bacterial infection inducing autoimmunity in rheumatoid arthritis. | en_GB |
dc.title | Bronchiectasis is a model for chronic bacterial infection inducing autoimmunity in rheumatoid arthritis. | en_GB |
dc.type | Article | en_GB |
dc.date.available | 2015-09-14T08:21:30Z | |
dc.identifier.issn | 2326-5191 | |
dc.description | Article | en_GB |
dc.description | Copyright © 2015 The Authors. Arthritis & Rheumatology is published by Wiley Periodicals, Inc. on behalf of the American College of Rheumatology. | en_GB |
dc.identifier.eissn | 2326-5205 | |
dc.identifier.journal | Arthritis and Rheumatology | en_GB |