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Mol Vis. 2017 Apr 12;23:219-227. eCollection 2017.

UVB promotes the initiation of uveitic inflammatory injury in vivo and is attenuated by UV-blocking protection.

Shao YC1,2, Liou JC1,2,3, Kuo CY4, Tsai YS2,5, Lin EC5,6, Hsieh CJ6,7, Lin SP2,5, Chen BY1,2,5.

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Department of Ophthalmology, Chung Shan Medical University Hospital, Taichung, Taiwan.
Department of Optometry, Chung Shan Medical University, Taichung, Taiwan.
Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Institute of Systems Biology and Bioinformatics, National Central University, Jhongli, Taiwan.
Institute of Optometry, Chung Shan Medical University, Taichung, Taiwan.
Department of Ophthalmology, Taipei City Hospital, Taipei, Taiwan.
Department of Optometry, University of Kang Ning, Taipei, Taiwan.



Uveitic inflammatory injury can cause irreversible visual loss; however, no single animal model recapitulates all the characteristics of human uveitis. Ultraviolet radiation (UVR) is one of the risk factors for uveitis, but the role of UVR in the pathogenesis of uveitic injury is unclear. The aim of this study was to elucidate whether UVB promotes the initiation of, and subsequently contributes to, uveitic inflammatory injury.


Mice were assigned to either a blank control group or one of three UVB treatment groups: no protection, protection with Nelfilcon A contact lens (Food and Drug Administration [FDA] class II, about 46.8% UVB transmittance), or protection with Etafilcon A contact lens (FDA class IV, about 0.55% UVB transmittance). The contact lenses acted as blocking barriers against UVR. After the application of UVR, pathologic injuries were determined with slit-lamp microscopy and histologic examination.


Compared with the intact status of the controls, the anterior eyes of the UVB groups showed pathologic alterations in physiologic properties and tissue integrity. UVR promoted anterior uveitic inflammatory injury, with expansion of the hyperemic iris vessels, over-production of aqueous humor protein, disruption of the blood-aqueous barrier, and embedding of infiltrative leukocytes inside the iridocorneal angle. However, blockage of UVR in vivo retarded the progression of uveitic inflammatory injury. The highest level of UV protection in the Etafilcon A group resulted in greater inhibition of uveitic inflammatory injury than that in the Nelfilcon A group.


This study demonstrates that UVB initiated and promoted uveitic inflammatory injury. UV protection is needed for the clinical management of anterior uveitis. The Etafilcon A lenses provide better protection of the anterior segment of the eye against UVB damage compared with the Nelfilcon A lenses.

[Indexed for MEDLINE]
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