S100B‐induced microglial and neuronal IL‐1 expression is mediated by cell type‐specific transcription factors

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<jats:title>Abstract</jats:title><jats:p>Both the astrocytic cytokine S100B and the pro‐inflammatory interleukin‐1 (IL‐1) are elevated in Alzheimer's disease, and each has been implicated in Alzheimer‐related neuropathology. We examined the gene‐regulatory events through which S100B induces IL‐1β expression. In primary microglia, S100B activated the transcription factors Sp1 and NFκB, followed by an increase in IL‐1β mRNA levels. The latter was blocked by a peptide inhibitor of NFκB or by a double‐stranded oligonucleotide containing a NFκB‐binding site to serve as ‘decoy’ DNA and reduce available NFκB. But in primary cortical neurons, decoy and siRNA experiments indicated that the IL‐1β induction by S100B was mediated by Sp1 without evidence of a role for NFκB. Our results suggest that the elevation of S100B and IL‐1 in Alzheimer brain and consequent neurodegenerative events are mediated through cell‐type specific gene‐regulatory events, providing mechanistic insight into connections between glial activation and neuronal dysfunction.</jats:p>

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