ArticleThe ocular surface2025
Destructive and protective effects and therapeutic targets of IL-36 family cytokines in dry eye disease.
Article in The ocular surface, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Recombinant IL-38 Alleviates Temporomandibular Joint Synovial Inflammation via IL-1R1-NF-κB-IL1β Pathway.International dental journal · 2026Article
- Investigating the role of the bacterial metabolite ectoine on immune regulation within the bovine female reproductive tract.Journal of animal science · 2026Article
- Protective Effects ofJournal of microbiology and biotechnology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
purposeTo explore the destructive and protective effects and therapeutic targets of IL-36 cytokines in dry eye disease using a murine dry eye model.
methodsA dry eye model was established in C57BL/6 mice exposed to desiccating stress (DS) with untreated mice as controls. A topical challenge model was performed in normal mice with exogenous rmIL-36α, rhIL-38 and 2 % ectoine, or PBS vehicle. IL-36 cytokine expression was assessed by RT-qPCR and immunofluorescent (IF) staining. Corneal epithelial damage was evaluated by corneal smoothness score, Oregon Green Dextran (OGD) fluorescent staining, and tight junction barrier.
resultsAll members of the IL-36 family were expressed by murine ocular surface epithelium. The expression of IL-36α and IL-36γ was upregulated while IL-38 and IL-36RN were down regulated in ocular surface of dry eye mice. A topical challenge of rmIL-36α directly destructed corneal surface with distorted smoothness, increased OGD uptake and IF intensity, and disrupted tight junction proteins ZO-1 and occludin. Co-application with rhIL-38 prevented all these corneal damages by rmIL-36α. Ectoine treatment reversed the pathological expression pattern of IL-36 cytokines, protected corneal epithelium from defects, and restored the tight junction barrier in DS mice, and even prevented corneal damage by rmIL-36α.
conclusionsOur findings demonstrate the upregulated pro-inflammatory agonists IL-36α and IL-36γ with downregulated antagonists IL-38 and IL-36RA in dry eye model, which provides a previously unknown mechanism and therapeutic targets in dry eye disease. The therapeutic efficacy of ectoine may be through reversing the pathological alteration of IL-36 cytokines in dry eye mice.
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