Maternal IgG Affects Brain Development of Mouse Pups
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1043197 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26894760_1.fastq.gz | Fastqsanger.gz | |||
| SRR26894760_2.fastq.gz | Fastqsanger.gz | |||
| SRR26894761_1.fastq.gz | Fastqsanger.gz | |||
| SRR26894761_2.fastq.gz | Fastqsanger.gz | |||
| SRR26894762_1.fastq.gz | Fastqsanger.gz |
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Project description:Maternal IgG is an immunoglobulin present in breast milk and has been shown to play a role in the development of the immune system in infants. The aim of this study was to investigate the effects of maternal IgG on brain development in mouse pups. Maternal IgG immunoreactivity was observed in microglial cells of the pup brain, peaking at postnatal 8 day. In particular, strong IgG immunoreactivity was observed in the microglia in the corpus callosum and cerebellar white matter. IgG stimulation of primary cultured microglia resulted in activation of the type I interferon feedback loop by Syk. Among the IgG subclasses, IgG2a was found to have a strong influence on microglia. Analysis of FcRn KO mice that were unable to take up IgG from their mothers revealed that these mice had abnormalities in the proliferation and/or survival of microglia, oligodendrocytes, and some types of interneurons. FcRn KO mice also exhibited abnormalities in social behavior and adaptation to novel environments. This study suggests that maternal IgG affects brain development in pups.
2024-05-24 | GSE248310 | GEO
Project description:Docosahexaenoic acid (DHA) is well known to promote visual and brain development while its protective effect on intestinal development in early life remains unknown. In order to understand the underlying biological effects of maternal DHA supplementation during lactation on the intestinal development of pups, we analyzed the proteomics of jejunum tissues from three groups with the DIA-MS method.
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Project description:The postnatal development of the mouse is characterized by a stress hyporesponsive period (SHRP), where basal corticosterone levels are low and responsiveness to mild stressors is reduced. Maternal separation is able to disrupt the SHRP and is widely used to model early trauma. In this study we aimed at identifying of brain systems involved in acute and possible long-term effects of maternal separation. We conducted a microarray-based gene expression analysis in the hypothalamic paraventricular nucleus after maternal separation, which revealed 52 differently regulated genes compared to undisturbed controls, among them are 37 up-regulated and 15 down-regulated genes. One of the prominently unregulated genes, angiotensinogen, was validated using a in-situ hybridization. Angiotensinogen is the precursor of angiotensin II the main effector of the brain renin-angiotensin system (RAS), which is known to be involved in stress system modulation in adult animals. Using the selective angiotensin type I receptor (AT(1)) antagonist candesartan we found strong effects on CRH and GR mRNA expression in the brain and ACTH release following maternal separation. AT(1) receptor blockade appears to enhance central effects of maternal separation in the neonate, suggesting a suppressing function of brain RAS during the SHRP. Taken together, our results illustrate the molecular adaptations that occur in the paraventricular nucleus following maternal separation and identify signaling cascades, that control stress system activity in the neonate. Keywords: phenotype Litters were randomly assigned to either a maternally non-separated or 24 hour maternally separated condition. At the time of testing, all pups from a litter were sacrificed immediately by decapitation.
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Project description:The transplacental transfer of maternal IgG to the developing fetus is critical for infant protection against infectious pathogens in the first year of life. However, factors that modulate the transplacental transfer efficiency of maternal IgG that could be harnessed for maternal vaccine design remain largely undefined. HIV-infected women have impaired placental IgG transfer, yet the mechanism underlying this impaired transfer is unknown, presenting an opportunity to explore factors that contribute to the efficiency of placental IgG transfer. We measured the transplacental transfer efficiency of maternal HIV and other pathogen-specific IgG in historical U.S. (n=120) and Malawian (n=47) cohorts of HIV-infected mothers and their HIV58 exposed uninfected and HIV-infected infants. We then examined the role of maternal HIV disease progression, infant factors, placental Fc receptor expression, and IgG Fc region subclass and glycan signatures and their association with transplacental transfer efficiency of maternal antigen-specific IgG. We established 3 distinct phenotypes of placental IgG transfer efficiency in HIV-infected women, including: 1) efficient transfer of the majority of antigen-specific IgG populations; 2) generally poor IgG transfer phenotype that was strongly associated with maternal CD4+ T cell counts, hypergammaglobulinemia, and frequently yielded non-protective levels of vaccine-specific IgG; and 3) variable transfer of IgG across distinct antigen specificities. Interestingly, maternal IgG characteristics, such as binding to placentally expressed Fc receptors FcgRIIa and FcgRIIIa, IgG subclass frequency, and Fc region glycan profiles were associated with placental IgG transfer efficiency. These maternal IgG transplacental transfer determinants were distinct among different antigen-specific IgG populations. Our findings suggest that in HIV-infected women, both maternal disease progression and Fc region characteristics modulate the selective placental transfer of distinct IgG subpopulations, with implications for both the health of HIV-exposed uninfected infants and maternal vaccine design.
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2013-09-09 | E-GEOD-45607 | biostudies-arrayexpress
Project description:Studies have indicated that altered maternal micronutrients and vitamins influence the development and susceptibility of newborns to chronic diseases. Among these, folic acid (FA) plays a key role in the synthesis and repair of DNA, along with maintenance of epigenetic DNA methylation. Deficiency of FA has been associated with the pathogenesis of neural tube defects. Since FA can modulate DNA methylation and affect gene expression, we investigated the effect of gestational FA supplementation on the expression of genes in the offspring brain. Our results suggest that a maternal ten-fold increase in FA supplementation alters the expression and dysregulates a number of genes in the offspring brain, including many involved in development. While a number of genes that were dysregulated were common to both male and female pups, there were sex differences in gene expression changes.
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Project description:The expression analysis of the brain of F1 pups, after maternal ingestion of 3,4-methylenedioxymethamphetamine (MDMA, 20mg/kg), resulted in significant transcriptional changes in both male and female pups.
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Project description:Maternal metabolic stress affects in vitro embryo's transcriptom pattern
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Project description:Folate is crucial for diverse biological processes including neurogenesis. While folate supplementation during pregnancy is standard for preventing neural tube defects (NTDs), concerns are growing over the potential risks of excessive maternal intake. In this study, we employed spatial transcriptomics and single-nucleus multi-omics techniques to investigate the impact of increased maternal folate intake on offspring brain development. Elevated folate intake broadly affected gene pathways linked to neurogenesis and neuronal axon myelination across multiple brain regions. Furthermore, specific gene expression alterations related to learning and memory processes emerged in thalamic and ventricular regions. Single-nucleus multi-omics analysis revealed that maturing excitatory neurons in dentate gyrus are particularly vulnerable to suboptimal maternal folate intake. Aberrant gene expression and chromatin accessibility changes were primarily centered on pathways governing ribosomal biogenesis, which is critical for synaptic formation. Altogether, our findings provide novel insights into how excessive maternal folate supplementation affects offspring brain development, notably by influencing gene expression and chromatin accessibility.
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