Dietary Omega-3 Fatty Acids Suppress Experimental Autoimmune Uveitis in Association with Inhibition of Th1 and Th17 Cell Function
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Shoda, Hiromi
Yanai, Ryoji
Yoshimura, Takeru
Nagai, Tomohiko
Kimura, Kazuhiro
Sobrin, Lucia
Sakoda, Yukimi
Tamada, Koji
Ikeda, Tsunehiko
Sonoda, Koh-Hei
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https://doi.org/10.1371/journal.pone.0138241Metadata
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Shoda, H., R. Yanai, T. Yoshimura, T. Nagai, K. Kimura, L. Sobrin, K. M. Connor, et al. 2015. “Dietary Omega-3 Fatty Acids Suppress Experimental Autoimmune Uveitis in Association with Inhibition of Th1 and Th17 Cell Function.” PLoS ONE 10 (9): e0138241. doi:10.1371/journal.pone.0138241. http://dx.doi.org/10.1371/journal.pone.0138241.Abstract
Omega (ω)–3 long-chain polyunsaturated fatty acids (LCPUFAs) inhibit the production of inflammatory mediators and thereby contribute to the regulation of inflammation. Experimental autoimmune uveitis (EAU) is a well-established animal model of autoimmune retinal inflammation. To investigate the potential effects of dietary intake of ω-3 LCPUFAs on uveitis, we examined the anti-inflammatory properties of these molecules in comparison with ω-6 LCPUFAs in a mouse EAU model. C57BL/6 mice were fed a diet containing ω-3 LCPUFAs or ω-6 LCPUFAs for 2 weeks before as well as after the induction of EAU by subcutaneous injection of a fragment of human interphotoreceptor retinoid-binding protein emulsified with complete Freund’s adjuvant. Both clinical and histological scores for uveitis were smaller for mice fed ω-3 LCPUFAs than for those fed ω-6 LCPUFAs. The concentrations of the T helper 1 (Th1) cytokine interferon-γ and the Th17 cytokine interleukin-17 in intraocular fluid as well as the production of these cytokines by lymph node cells were reduced for mice fed ω-3 LCPUFAs. Furthermore, the amounts of mRNAs for the Th1- and Th17-related transcription factors T-bet and RORγt, respectively, were reduced both in the retina and in lymph node cells of mice fed ω-3 LCPUFAs. Our results thus show that a diet enriched in ω-3 LCPUFAs suppressed uveitis in mice in association with inhibition of Th1 and Th17 cell function.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578775/pdf/Terms of Use
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