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Transcriptomic analysis of CD4+ Tcells from maternal immune activation (MIA) exposed offspring

ABSTRACT: Transcriptomic analysis of CD4+ Tcells from maternal immune activation (MIA) exposed offspring

PROVIDER: PRJNA695470 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13570968_1.fastq.gz	Fastqsanger.gz
	SRR13570968_2.fastq.gz	Fastqsanger.gz
	SRR13570969_1.fastq.gz	Fastqsanger.gz
	SRR13570969_2.fastq.gz	Fastqsanger.gz
	SRR13570970_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of CD4+ Tcells from maternal immune activation (MIA) exposed offspring

Project description:We report differentially regulated transcriptome of CD4+ T cells in MIA offspring

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Open chromatin analysis of CD4+ Tcells from maternal immune activation (MIA) exposed offspring

Project description:Open chromatin analysis of CD4+ Tcells from maternal immune activation (MIA) exposed offspring

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Open chromatin analysis of CD4+ Tcells from maternal immune activation (MIA) exposed offspring

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Embryonic and adult synaptic proteome analysis following maternal immune activation

Project description:Maternal infections during pregnancy pose an increased risk for neurodevelopmental psychiatric disorders (NPDs) in the offspring. Here, we examined age- and sex-dependent dynamic changes of the hippocampal synaptic proteome after viral-like maternal immune activation (MIA) in embryonic and adult mice.

2024-07-31 | PXD043094 | Pride

Maternal Immune Activation Disrupts Proteostasis in the Fetal Brain

Project description:Maternal infection and inflammation during pregnancy is associated with neurodevelopmental disorders in offspring, but little is understood about the molecular mechanisms underlying this epidemiologic phenomenon. We leveraged single-cell RNA sequencing to profile transcriptional changes in the rodent fetal brain in response to maternal immune activation (MIA) and identified perturbations in cellular pathways associated with mRNA translation, ribosome biogenesis, and stress signaling. We found that MIA specifically activated the integrated stress response (ISR) in male, but not female, MIA offspring, thereby reducing global mRNA translation and altering nascent proteome synthesis. Moreover, genetic blockade of ISR activation rescued the social behavior phenotype in MIA male offspring. Our data suggest that therapeutic targeting of the ISR may be beneficial in reducing maternal inflammation-associated neurodevelopmental disorders.

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Sex differences in offspring risk and resilience following 11β-hydroxylase antagonism in a rodent model of maternal immune activation

Project description:Maternal immune activation (MIA)puts offspring at greater risk for neurodevelopmental disorders associated with impaired social behavior. While it is known that immune signaling through the maternal, placental, and fetal compartments contribute to these phenotypical changes, it is unknown to what extent the stress response to illness is involved and how it can be harnessed for potential interventions. To this end, pregnant rat dams were treated with the clinically available 11β-hydroxylase inhibitor metyrapone, alongside administration of the bacterial mimetic lipopolysaccharide (LPS), on gestational day 15. Maternal, placental, and fetal CNS levels of corticosterone and placental 11ßHSD enzymes type 1 and 2 were measured 3-hrs post treatment. Subsequently, offspring social behaviors were measured across critical phases of development. MIA was associated with increased maternal, placental, and fetal CNS corticosterone concentrations that were diminished with metyrapone exposure. Metyrapone protected against reductions in placental 11ßHSD2 in males only, suggesting that less corticosterone was inactivated in female placentas. Behaviorally, metyrapone-exposure protected against MIA-induced social disruptions in juvenile, adolescent, and adult males, while females were unaffected or performed worse. Transcriptomic analyses revealed that metyrapone-exposure triggered opposing effects on gene expression to combat MIA-exposure in males, but not among females. Taken together, these findings illustrate that MIA-induced HPA responses act alongside the immune system to produce behavioral deficits. As a clinical drug already provided to pregnant people and neonates for the treatment of hypercortisolism, the sex-specific benefits and constraints of metyrapone should be investigated further as a potential means of reducing neurodevelopmental risks due to gestational MIA.

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Project description:Infection during pregnancy is strongly implicated as an environmental risk factor for autism spectrum disorder (ASD), with activation of the maternal immune system (MIA) identified in the causative pathway. Maternal exposure to viral and bacterial mimics at midgestation leads to the development of core ASD behaviors in rodent offspring. However, the fundamental pathogenic mechanisms coupling MIA to persistent changes in brain function and behavior are incompletely understood.The medial prefrontal cortex (mPFC) is a major locus of pathology in ASD and highly associated with behaviors dysregulated by MIA. Transcriptomic profiling of the mPFC from adult MIA and control offspring provides insight into molecular pathways persistently disrupted by prenatal exposure to maternal inflammation.

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