“…Briefly, whatever the inflammatory challenge applied on these cells (TLR3-4 or 7 agonists, Ab, interferon-g, hypoxia, or myelin), all studies reported a dose-dependent decrease in the production of proinflammatory factors (cytokines and/or chemokines) when treated with n-3 PUFAs (De Smedt-Peyrusse et al, 2008). N-3 PUFAs also inhibit the production and activity of the enzymes COX-2, iNOS, and the production of NO and reactive oxygen species (Moon et al, 2007;Lu et al, 2010;Antonietta Ajmone-Cat et al, 2012;Pettit et al, 2013;Chen et al, 2014;Corsi et al, 2015;Zendedel et al, 2015). This is correlated with a switch in microglial marker expression, from a proinflammatory to an anti-inflammatory phenotype (decreased CD40 and CD86, increased CD206) (Ebert et al, 2009;Chhor et al, 2013;Hjorth et al, 2013;Chen et al, 2014).…”