To maintain retinal homeostasis and preserve photoreceptor cells, harmful retinal inflammation must be controlled. Studies are now focusing on methods to control retinal inflammation, and this approach holds promise for RD treatment.
13–15 However, this approach should have minimum side effects because RD requires life-long therapy. In Japan, lecithin-bound iodine (LBI), considered an “old” drug, has been administered clinically for retinal diseases, including central serous chorioretinopathy, which causes serous retinal detachment (only Japanese reports). LBI was originally developed in 1955 for treating Graves’ disease in Japan. The administration of iodine agents or thyroid hormone agents was believed to enhance retinal metabolism.
16,17 The efficacy of LBI against retinal diseases was assessed in Japan (only Japanese reports); in the 1950s, LBI was widely prescribed for retinal diseases, including central serous chorioretinopathy, age-related macular degeneration, retinal detachment, and vitreous hemorrhage. However, with recent medical advancements and the development of surgical techniques, the frequency of LBI prescription has been decreasing steadily. Currently, LBI is prescribed mainly for patients with central serous chorioretinopathy. Recently, Sugimoto et al.
18 reported that LBI administration prevents hypoxic damage to RPE cells and suppresses CCL2 secretion from RPE cells in vitro. Elevation of the chemokine (C-C motif) ligand 2 (CCL2) expression is a common feature of inflammatory response in RD.
19 The expression of CCL2 in the retina and RPE is negligible in healthy young adult animals, but increases in acute inflammation and degeneration.
20 We hypothesized that the LBI-mediated prevention of inflammatory response in retina may attenuate RD in vivo. To test this hypothesis, in this study, we focused on LBI as a treatment agent for RD. For this, we used
Mertk−/−Cx3cr1GFP/+Ccr2RFP/+ mice.
21 This model develops RD owing to a lack of phagocytosis of photoreceptor outer segments by the RPE cells; in addition, CX3CR1 and CCR2 are labeled with fluorescein, which enables the observation of CX3CR1-positive microglia migration and CCR2-positive macrophage infiltration.
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