Abstract
Maternal immune activation (MIA) at the time of gestation has been linked to increased risk of neurodevelopmental psychiatric disorders. Animal and human models have been used to evaluate the relationship between MIA and these outcomes. Given that each of these two disciplines of study have their benefits and limitations, a translational perspective is expected to illuminate more than by the use of any single approach. In this article, we discuss this translational framework and explore how it may be enhanced by the utilization of epigenetic studies and by investigating the microbiome. In this perspectives piece, we focus on the impact of epidemiologic studies, animal models, and preclinical studies in the literature on MIA as well as the potential for greater integration between fields.
Highlights
Fetal developmental events occurring in utero are implicated in the postnatal health of offspring through adulthood
During Maternal immune activation (MIA), elevated interleukin-17a responses were caused by the activation of dendritic cells, a key cell type involved in Central nervous system (CNS) pathology, interacting with segmented filamentous bacteria (SFB) colonized Th17 cells [50]
This can be a potential factor for dysregulation of the hypothalamus–pituitary–adrenal gland (HPA) axis, which has been linked to the pathophysiology of schizophrenia [67]
Summary
Fetal developmental events occurring in utero are implicated in the postnatal health of offspring through adulthood. Environmental exposures during gestation, including maternal infection, nutritional deficiencies, toxic exposures, and other factors that cause stress during pregnancy are insidious during gestation. Central nervous system (CNS) disorders, schizophrenia, autism spectrum disorder (ASD), and bipolar disorder likely result from both genetic and environmental contributions. Epidemiologic studies have revealed strong connections between conditions associated with heighted maternal immune activation (MIA), resulting from infection and stress, and schizophrenia [1, 2], ASD [3, 4], and bipolar disorder [5] in offspring. More recent studies have begun to address potential mediating pathways including epigenetics, and the role of the microbiome in these disorders
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