{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T15:04:33Z","timestamp":1773155073529,"version":"3.50.1"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2021,11,16]],"date-time":"2021-11-16T00:00:00Z","timestamp":1637020800000},"content-version":"vor","delay-in-days":475,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"James Paget PhD Studentship"},{"DOI":"10.13039\/100007197","name":"U.S. Public Health Service","doi-asserted-by":"publisher","award":["5T32GM103702-05"],"award-info":[{"award-number":["5T32GM103702-05"]}],"id":[{"id":"10.13039\/100007197","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,9,14]]},"abstract":"<jats:title>Summary<\/jats:title>\n               <jats:p>Beh\u00e7et's disease (BD) is a vasculitis of unknown aetiology typified by chronic recurrent oral ulcers and systemic inflammatory manifestations. Neutrophils, and specifically their protease neutrophil elastase (NE), have been implicated in its pathology. Although NE is an effective anti-microbial, excessive NE can damage host tissue. Recurrent oral ulceration is a primary BD symptom, therefore we hypothesized that excessive neutrophil infiltration evidenced by increased NE and a reduction in specific endogenous inhibitors, secretory leucocyte protease inhibitor (SLPI) and alpha1-anti-trypsin (\u03b11AT) contributes to BD mucosal instability. NE, SLPI and \u03b11AT were quantified in saliva from BD patients with active oral ulcers (BDa) and quiet without ulcers (BDq), recurrent aphthous stomatitis (RASa; RASq) and healthy controls (HC). Although BDq saliva had marginally higher median NE levels (1112\u00a0ng\/ml) compared to both RASq (1043\u00a0ng\/ml) and HC (999\u00a0ng\/ml), SLPI was significantly reduced in BDq (P\u00a0&amp;lt;\u00a00\u00b701). Despite decreased SLPI protein, mRNA expression was significantly increased in BDq buccal epithelial swabs compared to RASq and HC (P\u00a0&amp;lt;\u00a00\u00b705, P\u00a0&amp;lt;\u00a00\u00b7001). NE remained enzymatically active, although \u03b11AT levels were at least eight times higher than SLPI in all groups, suggesting that \u03b11AT does not have a primary role in counteracting NE in saliva. Furthermore, NE levels in BDa patients medicated with both azathioprine (AZA) and colchicine (COLC) were significantly lower than those on COLC (P\u00a0=\u00a00\u00b70008) or neither (P\u00a0=\u00a00\u00b702), indicating that combining AZA\u00a0+\u00a0COLC may help to regulate excessive NE during ulceration. This study showed that enzymatically active NE coupled with reduced SLPI in BD saliva may contribute to recurrent oral ulcerations.<\/jats:p>","DOI":"10.1111\/cei.13483","type":"journal-article","created":{"date-parts":[[2020,6,24]],"date-time":"2020-06-24T21:07:21Z","timestamp":1593032841000},"page":"93-105","source":"Crossref","is-referenced-by-count":13,"title":["Neutrophil elastase and endogenous inhibitors in Beh\u00e7et's disease saliva"],"prefix":"10.1093","volume":"202","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7115-7545","authenticated-orcid":false,"given":"T","family":"Novak","sequence":"first","affiliation":[{"name":"Centre for Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK"},{"name":"Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F","family":"Fortune","sequence":"additional","affiliation":[{"name":"Centre for Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9843-4218","authenticated-orcid":false,"given":"L","family":"Bergmeier","sequence":"additional","affiliation":[{"name":"Centre for Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I","family":"Khan","sequence":"additional","affiliation":[{"name":"Centre for Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK"},{"name":"Department of Oral Pathology, Islamabad Medical and Dental College, Bharakahu, Islamabad, Pakistan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E","family":"Hagi-Pavli","sequence":"additional","affiliation":[{"name":"Centre for Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2020,7,29]]},"reference":[{"key":"2021121023213194300_cei13483-bib-0001","doi-asserted-by":"crossref","first-page":"1461","DOI":"10.1093\/rheumatology\/kel329","article-title":"Autoimmunity vs autoinflammation in Behcet's disease: do we oversimplify a complex disorder?","volume":"45","author":"Direskeneli","year":"2006","journal-title":"Rheumatology"},{"key":"2021121023213194300_cei13483-bib-0002","first-page":"291","article-title":"Behcet's disease: autoimmune or 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