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Neuroinflammation in utero may result in lifelong neurological disabilities.Astrocytes play a pivotal role, but the mechanisms are poorly understood. Noearly postnatal treatment strategies exist to enhance neuroprotective potentialof astrocytes. We hypothesized that agonism on alpha7 nicotinic acetylcholinereceptor (alpha7nAChR) in fetal astrocytes will augment their neuroprotectivetranscriptome profile, while the antagonistic stimulation of alpha7nAChR willachieve the opposite. Using an in vivo - in vitro model of developmentalprogramming of neuroinflammation induced by lipopolysaccharide (LPS), wevalidated this hypothesis in primary fetal sheep astrocytes cultures re-exposedto LPS in presence of a selective alpha7nAChR agonist or antagonist. Our RNAseqfindings show that a pro-inflammatory astrocyte transcriptome phenotypeacquired in vitro by LPS stimulation is reversed with alpha7nAChR agonisticstimulation. Conversely, antagonistic alpha7nAChR stimulation potentiates thepro-inflammatory astrocytic transcriptome phenotype. Furthermore, we conduct asecondary transcriptome analysis against the identical alpha7nAChR experimentsin fetal sheep primary microglia cultures and discuss the implications forneurodevelopment.

Alpha7 nicotinic acetylcholine receptor signaling modulates ovine fetal brain astrocytes transcriptome in response to endotoxin