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Circulating Clues in Ménière's Disease: Elevated Cell-Free DNA and a Pro-Inflammatory Signature in Patients' Blood
Marijana Sekulic1, Swethiny Kobivasan2, Stavros Giaglis1
1Department of Biomedicine, University Hospital Basel, 4031 Basel, Switzerland.
Abstract:
Ménière's disease (MD) is thought to involve dysfunction of the blood-labyrinth 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-1β, CCL3 (MIP-1α), 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-labyrinth 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.
Insights
Cell-free DNA (cfDNA) and inflammatory mediators in Ménière
Area of Science:
- Otolaryngology and Vascular Biology
Background:
- Ménière's disease (MD) is associated with blood-labyrinth barrier dysfunction, but the underlying mechanisms of endothelial injury are not fully understood.
- Circulating factors like cell-free DNA (cfDNA) and inflammatory mediators may play a role in vascular stress and barrier disruption in MD.
Purpose of the Study:
- To investigate the contribution of plasma cfDNA and inflammatory mediators to endothelial injury and blood-labyrinth barrier disruption in Ménière's disease.
Main Methods:
- Quantification of plasma cfDNA levels in MD patients and healthy controls.
- Assessment of endothelial barrier function using human stria vascularis endothelial cells exposed to patient plasma.
- Analysis of endothelial cytotoxicity, F-actin organization, syndecan-1 expression, and inflammatory mediator profiles (IL-1β, CCL3, CCL27).
Main Results:
- Significantly elevated cfDNA levels were found in MD patient plasma.
- MD plasma impaired endothelial barrier function, increased cytotoxicity, and caused glycocalyx degradation (reduced syndecan-1).
- DNase I treatment partially reversed these effects, highlighting cfDNA's role. Elevated IL-1β, CCL3, and CCL27 were observed in MD plasma.
Conclusions:
- Plasma cfDNA and inflammatory mediators cooperatively induce endothelial injury, cytoskeletal remodeling, and glycocalyx shedding, weakening the blood-labyrinth barrier in MD.
- Targeting cfDNA or preserving the glycocalyx may offer novel therapeutic strategies for Ménière's disease.
- cfDNA-based markers show potential for monitoring endothelial damage in MD.
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