Conjunctival Neuropathic and Inflammatory Pain-Related Gene Expression with Contact Lens Wear and Discomfort

• Published in: Ocular immunology and inflammation Vol. 29; no. 3; pp. 587 - 606
• Main Authors: López-de la Rosa, Alberto, Fernández, Itziar, García-Vázquez, Carmen, Arroyo-del Arroyo, Cristina, González-García, María J., Enríquez-de-Salamanca, Amalia
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 03.04.2021
• Subjects: Adult; Conjunctival Diseases - etiology; Conjunctival Diseases - genetics; contact lens; Contact Lenses, Hydrophilic - adverse effects; discomfort; Eye Pain - etiology; Eye Pain - genetics; Eye Proteins - genetics; Female; gene expression; Gene Expression Regulation - physiology; Humans; inflammation; Inflammation - etiology; Inflammation - genetics; Male; Neuralgia - etiology; Neuralgia - genetics; Pain; Pain Measurement; Prosthesis Fitting; RNA, Messenger - genetics; Young Adult; Pain; discomfort; inflammation; contact lens; gene expression
• ISSN: 0927-3948; 1744-5078
• DOI: 10.1080/09273948.2019.1690005

Purpose: To identify alterations in neuropathic and inflammatory pain gene expression associated with contact lens (CL) wear and CL discomfort (CLD). Methods: Eight non-wearers, eight asymptomatic CL wearers (CLWs) and eight symptomatic CLWs were included. Conjunctival cells were collected by impression cytology and the mRNA expression levels of 85 genes were analyzed. Differentially expressed genes between non-wearers and CLWs and between asymptomatic and symptomatic CLWs were analyzed. An enrichment analysis was also performed. Results: Twelve genes were upregulated (including IL10, PDYN and PENK) and 28 downregulated (CCL2, IL1A, IL1B, IL2 and NGF) in CLWs (p ≤ 0.050). Eleven genes were upregulated (CCL2, IL1A, IL1B, IL2 and NGF) and nine downregulated (PDYN and PENK) in symptomatic CLWs (p ≤ 0.035). Enriched overrepresented terms were related to pain, neuronal transmission and inflammation. Conclusion: Contact lens wear might produce a desensitization-like mechanism responsible for comfortable CL wear. A malfunction of this mechanism might contribute to CLD.