ArticleDevelopment (Cambridge, England)2024
Fetal brain response to maternal inflammation requires microglia.
Article in Development (Cambridge, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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Who cites it
29 citing papers in PubMed.
- Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development.Nature neuroscience · 2026Article
- Maternal immune activation disrupts epigenomic and functional maturation of cortical excitatory neurons.Molecular psychiatry · 2026Article
- The Motor Neuromuscular Axis: The Overlooked Element of Developmental Programming in Diabetes and Metabolic Syndrome.International journal of molecular sciences · 2026Review
- Prenatal stress alters offspring neurovascular, autonomic, and immune development in animal models of neuropsychiatric and cardiometabolic disorders.Journal of neuroendocrinology · 2026Review
- Microglia in systemic neuroimmune communication: functions beyond phagocytosis.Trends in immunology · 2026Review
- A mother's touch: microbial guardians of early immune imprinting.Trends in immunology · 2026Review
- Microglial Maturation and Functional Heterogeneity: Mechanistic Links to Neurodevelopmental Disorders.International journal of molecular sciences · 2026Review
- Vagus nerve stimulation as an anti-inflammatory therapy for maternal immune activation-induced alterations in offspring microglia and neurodevelopment.Frontiers in neuroscience · 2026Review
- Microglial activity during postnatal development is required for infantile amnesia in mice.PLoS biology · 2026Article
- The Nodding syndrome cerebrospinal fluid proteome: a lens into neurodevelopmental failure consistent with environmentally triggeredFrontiers in molecular neuroscience · 2026Article
- The potential role of aberrant microglial synaptic pruning in the neurodevelopmental pathogenesis of tourette syndrome.Frontiers in neuroscience · 2026Review
- Microglial colonization of the developing mouse brain is controlled by both microglial and neural CSF-1.The EMBO journal · 2026Article
- Gestational hypothyroxinemia causes an inflammatory environment at maternal-fetal tissues and fetal brain with impaired hippocampal dendritic spine maturation in the offspring.Scientific reports · 2025Article
- Microglial plasticity across development mediates infantile amnesia.bioRxiv : the preprint server for biology · 2025Article
- Does the Maternal Gut Microbiome Influence the Outcome of Perinatal Asphyxia?Antioxidants (Basel, Switzerland) · 2025Review
- Cannabidiol regulates apoptosis and glial cells homeostasis in the prefrontal cortex of offspring from obese rat mothers.Metabolic brain disease · 2025Article
- Microglia express Tie2 in a longitudinal imaging study of acute neural injury in mice.Molecular biology of the cell · 2025Article
- Inosine Treatment Attenuates White Matter Injury in Neonatal Rats Exposed to Maternal Inflammation.Neurochemical research · 2025Article
- CB1 and CB2 receptors differentially modulate the cognitive impact of maternal immune activation and perinatal cannabinoid exposure.Behavioural brain research · 2025Article
- Maternal Immune Activation Disrupts Epigenomic and Functional Maturation of Cortical Excitatory Neurons.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
In utero infection and maternal inflammation can adversely impact fetal brain development. Maternal systemic illness, even in the absence of direct fetal brain infection, is associated with an increased risk of neuropsychiatric disorders in affected offspring. The cell types mediating the fetal brain response to maternal inflammation are largely unknown, hindering the development of novel treatment strategies. Here, we show that microglia, the resident phagocytes of the brain, highly express receptors for relevant pathogens and cytokines throughout embryonic development. Using a rodent maternal immune activation (MIA) model in which polyinosinic:polycytidylic acid is injected into pregnant mice, we demonstrate long-lasting transcriptional changes in fetal microglia that persist into postnatal life. We find that MIA induces widespread gene expression changes in neuronal and non-neuronal cells; importantly, these responses are abolished by selective genetic deletion of microglia, indicating that microglia are required for the transcriptional response of other cortical cell types to MIA. These findings demonstrate that microglia play a crucial durable role in the fetal response to maternal inflammation, and should be explored as potential therapeutic cell targets.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.