Abstract
Purpose :
To identify alterations in the neuropathic and inflammatory pain gene expression of human conjunctival cells associated with contact lens (CL) discomfort
Methods :
Eight non-CL wearers and 16 soft CL wearers, further divided into 8 asymptomatic and 8 symptomatic CL wearers, as determined by the Contact Lens Dry Eye Questionnaire (CLDEQ) short form were included. Exclusion criteria were extended or continuous CL wear (overnight) and dry eye disease. The comfortable CL wearing time plus 2 hours was established as the CL wearing time for each symptomatic CL wearer subject before attending the examination visit. The CL wearing time of each asymptomatic CL wearer subject was paired one-by-one with that of the symptomatic group. Clinical assessment included visual acuity, tear break-up time (TBUT), fluorescein corneal staining and Schirmer test; additionally conjunctival epithelial cells were collected by impression cytology. Expression of 85 genes involved in neuropathic and inflammatory pain was analyzed by real-time RT-PCR with a commercial PCR array in mRNA extracted from cells. Differentially expressed genes between non-CL and CL wearers, and between asymptomatic and symptomatic CL wearers groups were analyzed. Enrichment analysis in Gene Ontology, KEGG pathways, and InterPro databases was performed to assign biological meaning to sets of genes found to be differentially expressed.
Results :
Twelve genes were upregulated and 28 downregulated in CL wearers compared to non-CL wearers: 11 genes were upregulated and 9 downregulated in the symptomatic CL wearers. Some of the upregulated genes in CL wearers included PDYNand PENKand IL-10, which are related to analgesia; conversely, these same genes were significantly downregulated in symptomatic CL wearer group compared to asymptomatic. These differentially expressed genes were overrepresented in several biological annotations, including terms related to pain, nerve transmission and inflammation among others.
Conclusions :
CL wear appears to produce a desensitization-like mechanism, mediated by the gene expression of several analgesic and inflammatory mediators, which may be responsible for a comfortable CL wear. An imbalance or malfunctioning of this mechanism could contribute to CL discomfort.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.