Abstract
Purpose:
To investigate the effect of Interleukin-17(IL-17) and IL-17 receptor (IL-17R) on ocular surface inflammation, we studied whether IL-17 stimulation can up-regulate inflammatory cytokines in corneal epithelial cells and fibroblast cells. We also analyzed the IL-17R expression in mouse alkali corneal burn model.
Methods:
Expression of IL-17R, IL-8, and CCL20 after stimulation by IL-17(100ng/ml) or tumor necrotizing factor(TNF)-α(50ng/ml) was investigated using human corneal epithelial cell line(HCE) and human corneal fibroblast cell line (HCF) by real-time reverse transcription polymerase chain reaction (RT-PCR).Unilateral eye of corneal alkali burn was made using filter paper presoaked in 1N NaOH using A/J mice. After the treatment, both eyes were enucleated on day 5. Two-μm-thick corneal section was made using laser assisted microdissection method and the amount of RNA in the samples was determined by real-time RT-PCR.
Results:
TNF-α stimulation increased significantly IL-17R, IL-8, and CCL20 expression in both HCE(1.7±0.2, 146.3±8.2, and 15.1±1.8times) and HCF(1.8±0.2 , 98.8±8.8, and 70.0±10.3 times ) compared to the non-treated control group(p<0.05, p<0.01,and p<0.01, respectively). On the other hand, IL-17 did not stimulate IL-17R expression significantly in both HCE and HCF, but increased IL-8 expression(2.9 ±0.5 and 7.1±1.0 )and CCL20 expression(2.9 ±0.5 and 3.9±0.4) significantly(p<0.01). IL-17R expression in alkali burned cornea increased by an average of 2.7 times compared with that of non-treated cornea.
Conclusions:
IL-17 and IL-17R play a role in pathophysiology of ocular surface inflammation.
Keywords: 480 cornea: basic science •
557 inflammation •
490 cytokines/chemokines