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• W1587065081 abstract "Abstract Glial‐secreted proinflammatory mediators are dynamically involved in central nervous system responses to exogenous stimuli such as infection, neurotoxins, and nerve injury. The therapeutic use of anti‐inflammatory agents may reduce certain central nervous system pathology induced by inflammatory responses. We investigated the role of interleukin (IL)‐4 in modulating the production of proinflammatory mediators from lipopolysaccharide‐stimulated mixed glia in vitro . Interestingly, IL‐4 significantly enhanced IL‐1β secretion and did not affect monocyte chemoattractant protein‐1 release, even though IL‐4 considerably inhibited IL‐6, tumor necrosis factor α, and nitric oxide production from rat neonatal mixed glia. Further, IL‐4 exhibited inhibitory effects on IL‐1β production in microglial‐enriched cultures, while significantly increasing IL‐1β production in microglial‐depleted glia. The enhancing effect of IL‐4 on IL‐1β production was found to be inversely correlated with the percentage of microglia present in the mixed glial population. In summary, IL‐4 did not act as a global anti‐inflammatory cytokine and in fact, under certain situations enhanced IL‐1β secretion. We conclude that IL‐4 exerts its anti‐inflammatory effects in a limited and target‐specific manner, which is delicately regulated by the cellular microenvironment. Therefore, precaution should be taken when clinically using IL‐4 to treat diseases manifested by overt inflammatory responses." @default.
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• W1587065081 date "2007-03-21" @default.
• W1587065081 modified "2023-10-18" @default.
• W1587065081 title "Induction of interleukin‐1β by interleukin‐4 in lipopolysaccharide‐treated mixed glial cultures: microglial‐dependent effects" @default.
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• W1587065081 doi "https://doi.org/10.1111/j.1471-4159.2007.04588.x" @default.
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