Valencia-Sandonís Cristina, Calderón-García Andrés Ángel, Blanco-Vázquez Marta, Valencia-Nieto Laura, Novo-Diez Andrea, Vázquez Amanda, Calonge Margarita, González-García María J, Enríquez-de-Salamanca Amalia
Institute of Applied Ophthalmobiology (IOBA), Universidad de Valladolid (UVa), Campus Miguel Delibes, Paseo de Belén 17, 47011 Valladolid, Spain.
Pain Unit, Alliance of University Hospitals, Health System of Castilla y León, Calle Dulzaina 2, 47012 Valladolid, Spain.
Int J Mol Sci. 2025 Sep 12;26(18):8918. doi: 10.3390/ijms26188918.
Dry eye disease (DED) is a prevalent condition characterized by ocular surface inflammation and pain. This study evaluated the long-term progression of DED by analyzing clinical and molecular status, considering the impact of chronic ocular pain. Patients with DED were evaluated at two visits (V1 and V2) separated by at least two years. Evaluations included validated symptom questionnaires alongside slit-lamp examination, corneal sensitivity testing, and sub-basal nerve plexus analysis. Basal tear samples were collected for multiplex quantification of 20 cytokines and substance P (SP), and conjunctival cells were obtained to analyze 25 genes and 12 microRNAs (miRNA). Based on the presence or absence of chronic ocular pain, patients were then divided into two groups. Patients improved in DED-related symptoms, with no changes observed in ocular surface signs. Corneal dendritic cell density decreased, along with epidermal growth factor (EGF), fractalkine, and monocyte chemoattractant protein (MCP-1) tear levels, whereas interleukin (IL)-10 and SP tear levels increased. Neurotrophic tyrosine kinase, receptor, type gene expression was significantly downregulated, especially in patients without chronic ocular pain. miR-665 expression decreased significantly in DED patients. Monitoring corneal dendritic cells, tear cytokines, and gene/miRNA expression offers promising tools for tracking DED progression. Distinguishing the presence of chronic ocular pain as a separate symptom is crucial to optimizing therapeutic strategies and DED progression.
干眼疾病（DED）是一种以眼表炎症和疼痛为特征的常见病症。本研究通过分析临床和分子状况，考虑慢性眼痛的影响，评估了DED的长期进展。对DED患者进行了两次至少相隔两年的随访（V1和V2）。评估包括经过验证的症状问卷以及裂隙灯检查、角膜敏感性测试和基底神经丛分析。收集基础泪液样本用于对20种细胞因子和P物质（SP）进行多重定量，并获取结膜细胞以分析25个基因和12种微小RNA（miRNA）。然后根据是否存在慢性眼痛将患者分为两组。DED相关症状有所改善，眼表体征未见变化。角膜树突状细胞密度降低，同时表皮生长因子（EGF）、趋化因子和单核细胞趋化蛋白（MCP-1）泪液水平降低，而白细胞介素（IL）-10和SP泪液水平升高。神经营养性酪氨酸激酶受体型基因表达显著下调，尤其是在无慢性眼痛的患者中。DED患者中miR-665表达显著降低。监测角膜树突状细胞、泪液细胞因子以及基因/miRNA表达为追踪DED进展提供了有前景的工具。将慢性眼痛作为一个单独的症状区分出来对于优化治疗策略和DED进展至关重要。
