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- W4313385512 abstract "Abstract It’s known that diabetics are more susceptible to infections and there is an association between diabetes and chronic inflammation, but whether systemic inflammation contributes to retinopathy remains unknown. Microglial-mediated inflammation has gained recognition as a key contributor to diabetic retinopathy (DR) pathogenesis. We have shown that signaling between the chemokine fractalkine (FKN) and CX3CR1 on microglia is important to maintain neuroprotection and that CX3CR1-deficiency directs microglial-mediated inflammation and neurotoxicity in the diabetic retina. To extend these studies, we tested the hypothesis that acute endotoxemia perpetuates microglial activation and that CX3CR1-deficent mice will be more susceptible to retinal pathology due to dysregulated microglial responses. Systemic endotoxemia was induced in nondiabetic and diabetic CX3CR1-HET and CX3CR1-KO mice by administration of four-daily injections of LPS (1 mg/kg/mouse; i.p.; n=12). Confocal analysis of retinal tissue revealed that in CX3CR1-KO mice, endotoxemia induced a robust-cellular activation represented by morphological changes, IL-1β, iNOS expression, and intense perivascular clusters of microglia. This phenotype was exacerbated in the diabetic CX3CR1-KO retina. These microglial lesions observed in CX3CR1-KO mice coincided with perivascular accumulation of the blood-protein fibrinogen. Lastly, fractalkine treatment (intraocular; 30 ng) into FKN-KO mice dampened microglial activation and astrogliosis during acute endotoxemia. These data suggest that systemic inflammation influences breakdown of the blood-retinal barrier, and may provide therapeutic advances by fractalkine treatment to mitigate DR pathogenesis." @default.
- W4313385512 created "2023-01-06" @default.
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- W4313385512 date "2016-05-01" @default.
- W4313385512 modified "2023-09-23" @default.
- W4313385512 title "Fractalkine signaling during systemic endotoxemia inhibits perivascular microglial lesion formation in the diabetic retina" @default.
- W4313385512 doi "https://doi.org/10.4049/jimmunol.196.supp.51.22" @default.
- W4313385512 hasPublicationYear "2016" @default.
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