Immune activation in the brains of fetal and adolescent mice
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ABSTRACT:
PROVIDER: PRJNA658356 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12486355_1.fastq.gz | Fastqsanger.gz | |||
| SRR12486355_2.fastq.gz | Fastqsanger.gz | |||
| SRR12486356_1.fastq.gz | Fastqsanger.gz | |||
| SRR12486356_2.fastq.gz | Fastqsanger.gz | |||
| SRR12486357_1.fastq.gz | Fastqsanger.gz |
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Project description:In order to investigate how the immune genes might be involved in the molecular mechanism underlying schizophrenia, we induced immune activation twice in mice, first time during mid-late fetal development stage by intraperitoneal injection (IPI) of lipopolysaccharide (LPS) in to the pregnant mice at G16 (16th day after gestation) and second time during puberty by IPI of LPS into the male offspring at P30 (30th day after birth), and carried out poly-A selected RNA-seq sequencing on the brain at P32 to evaluate transcriptional changes. We used saline as control for LPS, and set the experiments in three combination of saline and LPS treatments: (1) S-S (control group): saline at G16 + saline at P30; (2) L-S: LPS at G16 + saline at P30; (3) S-L: saline at G16 + LPS at P30; (4) L-L: LPS at G16 + LPS at P30.
2021-11-10 | GSE156568 | GEO
Project description:Background: There are critical molecular mechanisms that can be activated to induce myocardial repair and in humans this is most efficient during fetal development. The timing of heart development in relation to birth and the size/electrophysiology of the heart are similar in humans and sheep, providing a model to investigate the repair capacity of the mammalian heart and how this can be applied to adult heart repair. Methods: Myocardial infarction was induced by ligation of the left anterior descending coronary artery in fetal (105d gestation when cardiomyocytes are proliferative) and adolescent sheep (6 months of age when all cardiomyocytes have switched to an adult phenotype). An ovine gene microarray was used to compare gene expression in sham and infarcted (remote, border and infarct areas) cardiac tissue from fetal and adolescent hearts. Results: The gene response to myocardial infarction was less pronounced in fetal compared to adolescent sheep hearts and there were unique gene responses at each age. There were also region-specific changes in gene expression between each age, in the infarct tissue, tissue bordering the infarct, and tissue remote from the infarction. In total, there were 880 genes that responded to MI uniquely in the adolescent samples compared with 170 genes in the fetal response, as well as 742 overlap genes that showed concordant direction of change responses to infarction at both ages. Conclusions: In response to myocardial infarction, there were specific changes in genes within pathways of mitochondrial oxidation, muscle contraction, and haematopoietic cell lineages, suggesting that the control of energy utilisation and immune function are critical for effective heart repair. The more restricted gene response in the fetus may be an important factor in its enhanced capacity for cardiac repair.
2020-01-30 | GSE144509 | GEO
Project description:Maternal Immune Activation Disrupts Proteostasis in the Fetal Brain
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Project description:Activation of the maternal immune system during pregnancy can fetal development, which can lead to postnatal susceptibility to a wide range of diseases, including cardiovascular, metabolic and psychiatric disorders. During maternal immune activation (MIA), the maternal body must balance its ressources between mounting an immune response and investing resources into continued metabolism and growth : both essential for survival of the fetus and a successful pregnancy. How the placenta responds to MIA over time and how it can protect the fetus is not well understood, and neither are the fetal consequences of MIA. Here, we characterised the response to an induced acute inflammation in maternal lungs over time across maternal and fetal organs, using a combination of omics-methods, imaging and integrative computational analysis. We found that the placenta, unlike other maternal organs, did not react by inducing a typical inflammatory response, but instead initially induced genes associated to strengthen tissue integrity and simultaneously reduced growth to prevent exposure to potential infections. Afterwards, a return to homeostasis was observed, with heightened biosynthesis and expression of endoplasmic reticulum (ER) stress genes. This mechanism likely protects the fetus from inflammation, as we observed no immune response in the fetal liver transcriptome. Instead, we observed metabolic adaptations in the fetus, including a release of docosahexaenoic acid (DHA) Notably, DHA has a crucial function for fetal brain development , and levels of triglyceride and phosphatidylcholine lipids that are necessary for transportation of DHA to the brain were also increased. This metabolic response is likely a combination of the placental MIA response and temporary maternal fasting, caused by MIA-induced fever and lack of nutrient intake. Our study shows, for the first time, the temporal and systemic response to MIA in lungs across maternal and fetal organs.
2024-06-13 | PXD039402 | Pride
Project description:A mouse model of maternal immune activation (MIA) is commonly used to study neurodevelopmental disorders. Gene expression analysis has suggested that fetal brain macrophages may be activated by MIA, but it is unclear whether these transcriptional changes connect to behavioral phenotypes in offspring. Here, we have shown that the induction of autism spectrum disorder (ASD)-like behavioral phenotypes by MIA in male offspring is dependent upon fetal activation of the toll-like receptor 3 (TLR3) signaling molecule TRIF. Using single-cell RNA sequencing, we identified a cluster of border-associated macrophages (BAMs) that was significantly enriched in wild-type fetal brains following TLR3-MIA but not diminished in Trif -/- fetal brains. Moreover, after TLR3-MIA, the number of fetal BAMs in the choroid plexus, but not in the meninges, was increased, and these cells were characterized by increased S100a8/9 expression. Finally, we proposed that activation of fetal TLR3-TRIF signaling was induced by transplacental viral infection. Overall, our data suggest that fetal TLR3 signaling contributes to MIA-induced ASD-like behavioral phenotypes in mice.
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Project description:m6A profiling of early, adolescent, aged and Alzheimer brains
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Project description:Investigation of spatial transcriptomic responses of nonhuman primate fetal brains during development
2023-11-02 | GSE227533 | GEO
Project description:Activation of the maternal immune system during pregnancy affects fetal development, which can increase in postnatal susceptibility to a range of diseases, including cardiovascular, metabolic and psychiatric disorders. During maternal immune activation (MIA), the maternal body must balance its ressources between mounting an immune response and investing resources into continued metabolism and growth, essentials for survival of the fetus and a successful pregnancy. How the placenta responds to MIA over time and how it can protect the fetus is not well understood, and neither are the fetal consequences of MIA. Here, we characterised the response to acute maternal lung inflammation across time in maternal and fetal organs, using a combination of omics, imaging and integrative computational analyses. We found that the placenta, unlike other maternal organs, did not react by a typical innate immune response, but instead induced genes associated with increased tissue integrity, likely to prevent fetal exposure to potential infections, and simultaneously reduced expression of growth-associated genes. Subsequently, a return to homeostasis was observed, with heightened expression of biosynthesis and endoplasmic reticulum (ER) stress genes. These responses likely protect the fetus from inflammation, as we observed no immune response in the fetal liver transcriptome. Instead, we observed metabolic adaptations in the fetus, including a release of docosahexaenoic acid (DHA) carrying metabolites, including triglyceride and phosphatidylcholine. Notably, DHA is crucial for fetal brain development. This metabolic response is likely a combination of the placental MIA response and temporary maternal fasting, caused by MIA-induced fever and lack of nutrient intake. Our study shows, for the first time, the integrated temporal and systemic response to LPS in lungs across maternal and fetal organs
2024-02-01 | GSE224116 | GEO
Project description:Adult hematopoietic stem cells (HSCs) respond directly to inflammation and infection, resulting in both acute and persistent changes in quiescence, mobilization, and differentiation. Here we show that fetal HSCs respond to maternal inflammation in utero, and the fetal response drives long-term changes to postnatal hematopoiesis and immunity. Heterogeneous fetal hematopoietic stem and progenitor cells (HSPCs) show divergent responses to maternal immune activation (MIA), including changes in quiescence, expansion, and immune cell output. Single cell transcriptomic analysis of fetal HSPCs reveals specific upregulation of inflammation-responsive genes in discrete populations, in response to upregulated IFNα and IL-1α in the fetal liver cytokine milieu. Postnatally, MIA caused the inappropriate expansion and persistence of transient progenitors, concomitant with increased cellularity and hyper-responsiveness of fetal-derived immune cells. Our investigation demonstrates how inflammation in utero can direct the trajectory of hematopoiesis and immunity by reshaping fetal HSC establishment.
2023-01-27 | GSE161926 | GEO
Project description:Adult hematopoietic stem cells (HSCs) respond directly to inflammation and infection, resulting in both acute and persistent changes in quiescence, mobilization, and differentiation. Here we show that fetal HSCs respond to maternal inflammation in utero, and the fetal response drives long-term changes to postnatal hematopoiesis and immunity. Heterogeneous fetal hematopoietic stem and progenitor cells (HSPCs) show divergent responses to maternal immune activation (MIA), including changes in quiescence, expansion, and immune cell output. Single cell transcriptomic analysis of fetal HSPCs reveals specific upregulation of inflammation-responsive genes in discrete populations, in response to upregulated IFNα and IL-1α in the fetal liver cytokine milieu. Postnatally, MIA caused the inappropriate expansion and persistence of transient progenitors, concomitant with increased cellularity and hyper-responsiveness of fetal-derived immune cells. Our investigation demonstrates how inflammation in utero can direct the trajectory of hematopoiesis and immunity by reshaping fetal HSC establishment.
2023-01-27 | GSE161925 | GEO