Abstract
β-funaltrexamine differentially modulates chemokine and cytokine expression in normal human astrocytes and C20 human microglial cells
Highlights
Neuroinflammation is present in brain infection, trauma, neurodegenerative diseases, and psychiatric disorders as well[1,2,3,4,5]
IL-1β-induced interferon-γ inducible protein-10 (CXCL10) production in normal human astrocytes (NHA) was more sensitive to chronic (3 day) β-FNA as indicated by an approximately 3-fold lower EC50 compared to that observed in acutely treated cells
Chronic β-FNA did not affect IL-1β-induced monocyte chemoattractant protein-1 (CCL2) or IL-6 production in NHA. β-FNA inhibited phosphorylation of NF-κB p65, suggesting that the inhibitory effects may be due in part to reduced NF-κB activation
Summary
Neuroinflammation is present in brain infection, trauma, neurodegenerative diseases, and psychiatric disorders as well[1,2,3,4,5]. Astrocytes have a fundamental role in neuropathogenesis, in part, through the release of neurotoxic/neuroinflammatory factors including cytokines [i.e., interleukin (IL)-1β and IL-6] and chemokines [interferon-γ inducible protein-10 (CXCL10) and monocyte chemoattractant protein-1 (CCL2)]. These secreted factors can be directly neurotoxic or can induce further glial activation/dysregulation[14,15,16,17]. Emerging evidence highlights the importance of astrocyte/microglia dysregulation in a wide range of CNS disorders, implicating glial cells as potential therapeutic targets[18,19,20,21]
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