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Highlights: [•] Immune function of glial cells under glucose-deprivation was investigated. [•] PGE2 +IFNγ-induced IL-6 production was enhanced under glucose-deprived condition. [•] PGE2 +IFNγ-induced iNOS expression was attenuated under glucose-deprived condition. [•] ER stress was involved in glucose-deprivation-induced IL-6 production. [•] Activation of glial cells under glucose starvation protected neuronal cell death. [Copyright &y& Elsevier]

Glucose metabolism plays central role in maintaining brain function. Under ischemic condition, where glucose levels were reduced, glial cells induce pro-inflammatory cytokine production. In the present study, we found prostaglandin (PG) E2+interferon (IFN) γ-induced interleukin (IL)-6 production was enhanced under glucose-deprived condition in the primary cultured glial cells. On the other hand, to our surprise, we found that PGE2+IFNγ-induced iNOS expression was attenuated under glucose-deprived condition. These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition. By activating theses responses glial cells may protect neurons because we observed increased neuronal cell viability in the immune-activated glial cell conditioned medium. Overall, our results suggest a link between ER stress and immune reactions under glucose-deprived condition in the glial cells., (Copyright © 2013 Elsevier Inc. All rights reserved.)