Fetal brain response to maternal inflammation requires microglia [Maternal_Inflammation]
In utero infection and maternal inflammation can adversely impact fetal brain development. Maternal systemic illness, even in the absence of direct fetal central nervous system infection, is associated with an increased risk of autism and schizophrenia in affected offspring. The cell types mediating the response of the fetal brain to maternal inflammation are largely unknown, hindering the development of therapies to prevent and treat adverse neuropsychiatric outcomes. Here, we show that microglia are enriched for expression of receptors for relevant pathogens and cytokines throughout embryonic development. Overall design: We injected pregnant mice with either poly(I:C) to induce maternal immune activation, or saline controls. We isolated microglia from the somatosensory (S1) cortex of the pups at E13, E15, and P14, and performed single-cell RNA sequencing to asses microglial subtypes and response to maternal immune activation. We also performed single-nucleus RNA sequencing of the developing S1 cortex at E15.5 in Csf1r null mice and wild-type littermate controls after maternal poly(I:C) or saline injection at E12.5.