Title : Early life alcohol exposure primes hypothalamic microglia to later-life hypersensitivity to immune stress: possible epigenetic mechanism.

Pub. Date : 2019 Aug

PMID : 30737481






3 Functional Relationships(s)
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1 Exposure to neonatal alcohol resulted in acute increases in activation and inflammatory gene expression in hypothalamic microglia including tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). Alcohols interleukin 6 Homo sapiens
2 Exposure to neonatal alcohol resulted in acute increases in activation and inflammatory gene expression in hypothalamic microglia including tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). Alcohols interleukin 6 Homo sapiens
3 Investigation of possible epigenetic programming mechanisms by alcohol revealed neonatal alcohol decreased several repressive regulators of transcription in hypothalamic microglia, while concomitantly increasing histone H3 acetyl lysine 9 (H3K9ac) enrichment at TNF-alpha and IL-6 promoter regions. Alcohols interleukin 6 Homo sapiens