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Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [RNA-Seq]

ABSTRACT: Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [RNA-Seq]

PROVIDER: PRJNA679899 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13093885_1.fastq.gz	Fastqsanger.gz
	SRR13093885_2.fastq.gz	Fastqsanger.gz
	SRR13093886_1.fastq.gz	Fastqsanger.gz
	SRR13093886_2.fastq.gz	Fastqsanger.gz
	SRR13093887_1.fastq.gz	Fastqsanger.gz

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Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity

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Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [scRNA-Seq']

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.

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Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [RNA-Seq]

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Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [scRNA-Seq']

Project description:Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [scRNA-Seq']

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Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity

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Prenatal inflammation perturbs murine fetal hematopoietic development and causes persistent changes to postnatal immunity.

Project description:Adult hematopoietic stem and progenitor cells (HSPCs) respond directly to inflammation and infection, causing both acute and persistent changes to quiescence, mobilization, and differentiation. Here we show that murine fetal HSPCs respond to prenatal inflammation in utero and that the fetal response shapes postnatal hematopoiesis and immune cell function. Heterogeneous fetal HSPCs show divergent responses to maternal immune activation (MIA), including changes in quiescence, expansion, and lineage-biased output. Single-cell transcriptomic analysis of fetal HSPCs in response to MIA reveals specific upregulation of inflammatory gene profiles in discrete, transient hematopoietic stem cell (HSC) populations that propagate expansion of lymphoid-biased progenitors. Beyond fetal development, MIA causes the inappropriate expansion and persistence of fetal lymphoid-biased progenitors postnatally, concomitant with increased cellularity and hyperresponsiveness of fetal-derived innate-like lymphocytes. Our investigation demonstrates how inflammation in utero can direct the output and function of fetal-derived immune cells by reshaping fetal HSC establishment.

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Genome-wide postnatal changes in immunity following fetal inflammatory response

Project description:The fetal inflammatory response (FIR) increases the risk of perinatal brain injury, particularly in extremely low gestational age newborns (ELGANs, < 28 weeks of gestation). One of the mechanisms contributing to such a risk is a postnatal intermittent or sustained systemic inflammation (ISSI) following FIR. The link between prenatal and postnatal systemic inflammation is supported by the presence of well-established inflammatory biomarkers in the umbilical cord and peripheral blood. However, the extent of molecular changes contributing to this association is unknown. Using RNA sequencing and mass spectrometry proteomics, we profiled the transcriptome and proteome of archived neonatal dried blood spot (DBS) specimens from 21 ELGANs. Comparing FIR-affected and unaffected ELGANs, we identified 782 gene and 27 protein expression changes of 50% magnitude or more, and an experiment-wide significance level below 5% false discovery rate. These expression changes confirm the robust postnatal activation of the innate immune system in FIR-affected ELGANs and reveal for the first time an impairment of their adaptive immunity. In turn, the altered pathway provide clues about the molecular mechanisms triggering ISSI after FIR, and the onset of perinatal brain injury.

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