A dataset of the effects of maternal dietary choline supplementation as a potential prophylactic to protect against the embryonic effects of prenatal air pollution
Air pollution causes widespread inflammatory changes in the body and brain. These changes are linked to neurocognitive difficulties, increased anxiety and depression, and increased prevalence of neurodegenerative disorders. When exposure to air pollution occurs early in development, children exhibit impaired working memory ability (Sunyer et al., 2015). In addition, prenatal exposure to diesel particulate matter (DEP) increases inflammatory cytokine expression in the whole brain of embryonic day 18 (E18) males and leads to adverse long-term negative outcomes (Bolton et al., 2012). In contrast, dietary choline supplementation is negatively correlated with inflammatory cytokine production in adult rats and cultured human cells (Zhang et al., 2018; Jiang et al., 2014). When administered as a supplement to pregnant rats, choline also improves working memory in adulthood (Meck et al., 2008; Meck & Williams, 1999; 1997). The current study sought to determine if prenatal dietary choline supplementation protects against the effects of air pollution in the developing brain and in the placenta and fetal liver. These data revealed region-specific microglial morphology alterations in fetal brain and in inflammatory gene expression in the placenta and fetal liver (specifically, TNF, TLR2, TLR4, ITGAM) due to maternal choline supplementation and/or maternal air pollution exposure. We found that DEP led to changes in microglial morphology in the fetal dentate gyrus of E18 male, but not female, fetuses. Choline supplementation partially prevented this change in microglial morphology to an increase in “round”/ameboid morphology. Interestingly, these effects were region-specific: the opposite pattern was seen in the PVN, and no diesel effect was observed in the amygdala and parietal cortex. In the placenta and fetal liver of males, inflammatory gene expression was affected by both air pollution and maternal choline supplementation. However, maternal choline supplementation alone upregulated inflammatory gene expression in females, which may indicate an alteration in maturation rate. These data further contribute to the growing literature indicating region- and tissue-specificity in the developmental immune system in the context of maternal exposures.