PURPOSE: To investigate whether unilateral in vivo UVR-B exposure of one eye affects the fellow eye in a co-cataractogenic, sympathetic reaction and to determine whether an inflammatory response could be involved in the pathogenesis. METHODS: C57BL/6 mice were unilaterally exposed in vivo to UVR-B for 15 min. In the group of 24 animals each received 0×/2×/3×/or 4× cataract threshold equivalent dose. Following 48-hr UVR-B exposure, cataract morphology was documented in dark-field illumination photography, and light scattering was quantified, in both lenses in vitro. Serum levels of pro-inflammatory cytokines IL-1ß, IL-6 and TNF-α were analysed with ELISA. Immunohistochemistry was performed for inflammatory infiltration in exposed and contralateral eyes. RESULTS: UVR-B exposure induced cataract in all exposed lenses. There was additionally a significant UVR dose-dependent increase in light scattering in the lenses of the non-exposed fellow eye. Inflammatory infiltration was detected immunohistochemically in the anterior segment of both eyes. IL-1β serum concentration increased with increasing UVR-B exposure dose. There was a similar trend for serum IL-6 but not for TNF-α. CONCLUSION: Unilateral UVR-B exposure to one eye is associated with intraocular inflammation and an increase in lens light scattering also in the unexposed, fellow eye. A resulting systemic inflammatory response might be mediated by IL-1β and possibly IL-6. The finding that an inflammatory response may play a role in UVR-B-induced cataract development might initiate new strategies in the prevention of the disease.
PURPOSE: To investigate whether unilateral in vivo UVR-B exposure of one eye affects the fellow eye in a co-cataractogenic, sympathetic reaction and to determine whether an inflammatory response could be involved in the pathogenesis. METHODS: C57BL/6 mice were unilaterally exposed in vivo to UVR-B for 15 min. In the group of 24 animals each received 0×/2×/3×/or 4× cataract threshold equivalent dose. Following 48-hr UVR-B exposure, cataract morphology was documented in dark-field illumination photography, and light scattering was quantified, in both lenses in vitro. Serum levels of pro-inflammatory cytokines IL-1ß, IL-6 and TNF-α were analysed with ELISA. Immunohistochemistry was performed for inflammatory infiltration in exposed and contralateral eyes. RESULTS: UVR-B exposure induced cataract in all exposed lenses. There was additionally a significant UVR dose-dependent increase in light scattering in the lenses of the non-exposed fellow eye. Inflammatory infiltration was detected immunohistochemically in the anterior segment of both eyes. IL-1β serum concentration increased with increasing UVR-B exposure dose. There was a similar trend for serum IL-6 but not for TNF-α. CONCLUSION: Unilateral UVR-B exposure to one eye is associated with intraocular inflammation and an increase in lens light scattering also in the unexposed, fellow eye. A resulting systemic inflammatory response might be mediated by IL-1β and possibly IL-6. The finding that an inflammatory response may play a role in UVR-B-induced cataract development might initiate new strategies in the prevention of the disease.