{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T12:13:44Z","timestamp":1771416824902,"version":"3.50.1"},"reference-count":52,"publisher":"MDPI AG","issue":"4","license":[{"start":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T00:00:00Z","timestamp":1771372800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Thomas und Elsbeth Stitzinger-Stiftung"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>M\u00e9ni\u00e8re\u2019s disease (MD) is thought to involve dysfunction of the blood\u2013labyrinth barrier, but circulating mechanisms of endothelial injury remain poorly understood. The present study investigated whether cell-free DNA (cfDNA) and inflammatory mediators in plasma contribute to vascular stress and barrier disruption in MD. cfDNA levels were significantly elevated in plasma from patients compared with plasma from healthy controls. Exposure of primary human stria vascularis endothelial cell monolayers to plasma from MD patients led to decreased transepithelial electrical resistance and a significant increase in FITC-dextran permeability, indicating impaired barrier function. MD plasma also induced higher lactate dehydrogenase release and pronounced F-actin disorganization with reduced syndecan-1 expression, consistent with endothelial cytotoxicity and glycocalyx degradation. DNase I partially reversed these effects, implicating extracellular DNA as a key driver. Furthermore, IL-1\u03b2, CCL3 (MIP-1\u03b1), and CCL27 were elevated in MD plasma. Collectively, our data support a model in which cfDNA and inflammatory mediators cooperatively induce endothelial injury, cytoskeletal remodeling, and glycocalyx shedding, leading to blood\u2013labyrinth barrier weakening. Targeting extracellular DNA or glycocalyx preservation may represent a novel strategy to protect inner ear vascular integrity and modify disease progression in MD, and cfDNA-related readouts may be promising biomarkers of endothelial damage.<\/jats:p>","DOI":"10.3390\/ijms27041948","type":"journal-article","created":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T11:45:58Z","timestamp":1771415158000},"page":"1948","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Circulating Clues in M\u00e9ni\u00e8re\u2019s Disease: Elevated Cell-Free DNA and a Pro-Inflammatory Signature in Patients\u2019 Blood"],"prefix":"10.3390","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3761-7253","authenticated-orcid":false,"given":"Marijana","family":"Sekulic","sequence":"first","affiliation":[{"name":"Department of Biomedicine, University Hospital Basel, 4031 Basel, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Swethiny","family":"Kobivasan","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, University of Basel, 4056 Basel, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2216-9539","authenticated-orcid":false,"given":"Stavros","family":"Giaglis","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, University Hospital Basel, 4031 Basel, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel","family":"Bodmer","sequence":"additional","affiliation":[{"name":"Otorhinolaringology Department, University Hospital Basel, 4031 Basel, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vesna","family":"Petkovic","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, University Hospital Basel, 4031 Basel, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2026,2,18]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"529","DOI":"10.1016\/S0030-6665(02)00019-1","article-title":"Etiology, pathophysiology of symptoms, and pathogenesis of Meniere\u2019s disease","volume":"35","author":"Paparella","year":"2002","journal-title":"Otolaryngol. 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