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SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

ABSTRACT: SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

PROVIDER: PRJNA719365 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14134832.fastq.gz	Fastqsanger.gz
	SRR14134833.fastq.gz	Fastqsanger.gz
	SRR14134834.fastq.gz	Fastqsanger.gz
	SRR14134835.fastq.gz	Fastqsanger.gz
	SRR14134836.fastq.gz	Fastqsanger.gz

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SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

Project description:Pregnant women appear to be at increased risk for severe outcomes associated with COVID-19, but the pathophysiology underlying this increased morbidity and its potential impact on the developing fetus is not well understood. In this study of pregnant women with and without COVID-19, we assessed viral and immune dynamics at the placenta during maternal SARS-CoV-2 infection. Amongst uninfected women, ACE2 was detected by immunohistochemistry in syncytiotrophoblast cells of the normal placenta during early pregnancy but was rarely seen in healthy placentas at full term. Term placentas from women infected with SARS-CoV-2, however, displayed a significant increase in ACE2 levels. Using immortalized cell lines and primary isolated placental cells, we determined the vulnerability of various placental cell types to direct infection by SARS-CoV-2 in vitro. Yet, despite the susceptibility of placental cells to SARS-CoV-2 infection, viral RNA was detected in the placentas of only a subset (∼13%) of women in this cohort. Through single cell transcriptomic analyses, we found that the maternal-fetal interface of SARS-CoV-2-infected women exhibited markers associated with pregnancy complications, such as preeclampsia, and robust immune responses, including increased activation of placental NK and T cells and increased expression of interferon-related genes. Overall, this study suggests that SARS-CoV-2 is associated with immune activation at the maternal-fetal interface even in the absence of detectable local viral invasion. While this likely represents a protective mechanism shielding the placenta from infection, inflammatory changes in the placenta may also contribute to poor pregnancy outcomes and thus warrant further investigation.

2021-04-03 | GSE171381 | GEO

SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

Project description:Pregnant women appear to be at increased risk for severe outcomes associated with COVID-19, but the pathophysiology underlying this increased morbidity and its potential impact on the developing fetus is not well understood. In this study of pregnant women with and without COVID-19, we assessed viral and immune dynamics at the placenta during maternal SARS-CoV-2 infection. Viral RNA was only rarely detected in the placentas from SARS-CoV-2-positive women in our cohort, with only 1/11 positive for infection at the maternal-fetal interface. Through bulk RNA transcriptomic analyses, we found that placentas from SARS-CoV-2-positive pregnancies exhibited inflammatory markers of immune activation, even in the majority of samples which did not show local invasion of the virus. These markers are associated with pregnancy complications such as preeclampsia and poor fetal outcomes. Overall, this study suggests that SARS-CoV-2 is associated with immune activation at the maternal-fetal interface even in the absence of detectable local viral invasion. While this likely represents a protective mechanism shielding the placenta from infection, inflammatory changes in the placenta may also contribute to poor pregnancy outcomes and thus warrant further investigation.

2021-04-14 | GSE171995 | GEO

SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

Project description:SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

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Single-cell analysis reveals transcriptomic and epigenomic impacts on the maternal-fetal interface upon SARS-CoV-2 infection

Project description:The involvement of epigenetic regulation of cis-regulatory elements and retrotransposons in the maternal-fetal interface of COVID-19-related pregnancy complications.

2023-05-02 | E-MTAB-11749 | biostudies-arrayexpress

Sexually dimorphic crosstalk at the maternal-fetal interface

Project description:The first trimester is a critical window of maternal-fetal communication for pregnancy. RNA-sequencing of matched maternal decidua (4) and placenta (4) identified 91 sexually dimorphic receptor-ligand pairs across the maternal-fetal interface, 32 in females and 59 in males.

2020-08-20 | GSE131874 | GEO

Sexually dimorphic crosstalk at the maternal-fetal interface

Project description:The first trimester is a critical window of maternal-fetal communication for pregnancy. Using single cell RNA-sequencing to dissect placenta heterogeneity, we identified five major cell types (trophoblasts, stromal cells, hofbauer cells, antigen presenting cells and endothelial cells). We identified seven unique trophoblast subclusters, including new subtypes that transition into the terminal cell types, extra-villous trophoblasts and syncytiotrophoblasts. As fetal sex impacts pregnancy, we analyzed sex differences in each cell type and identified differences in immune cell function. TGFβ1, β-estradiol, and dihydrotestosterone emerge as upstream regulators of sexually dimorphic genes in a cell type specific manner. Thus, the fetal contribution at the maternal-fetal interface is cell and sex specific.

2020-08-20 | GSE131696 | GEO

Single-cell analysis reveals transcriptomic and epigenomic impacts on the maternal-fetal interface upon SARS-CoV-2 infection

Project description:During pregnancy, the maternal-fetal interface plays vital roles in fetal development. Its disruption is frequently found in pregnancy complications. Recent works show increased incidences of adverse pregnancy outcomes in COVID-19 patients; however, the mechanism remains unclear. Here, we analyzed the molecular impacts of SARS-CoV-2 infection on the maternal-fetal interface. Generating bulk and single-nucleus transcriptomic and epigenomic profiles from COVID-19 patients and control samples, we discovered aberrant immune activation and angiogenesis patterns in distinct cells from patients. Surprisingly, retrotransposons were also dysregulated in specific cell types. Notably, reduced enhancer activities of LTR8B elements were functionally linked to the downregulation of Pregnancy-Specific Glycoprotein genes in syncytiotrophoblasts. Our findings revealed that SARS-CoV-2 infection induced significant changes to the epigenome and transcriptome at the maternal-fetal interface, which may be associated with pregnancy complications.

| EGAS00001006263 | EGA

SARS-CoV-2 impacts the transcriptome and epigenome at the maternal-fetal interface during pregnancy

Project description:SARS-CoV-2 impacts the transcriptome and epigenome at the maternal-fetal interface during pregnancy

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Genome-wide expression profiling at maternal-fetal interface in case of recurrent miscarriage (RM)

Project description:Maternal-fetal interface plays a crucial role to ensure a successful pregnancy. RM (≥3 consecutive pregnancy losses) occurring in 1-3% of fertile couples has a heterogeneous background with contribution from both genetic and environmental factors. As several physiological processes are affected in the pathogenesis of RM, it serves as a good model to study the processes at the maternal-fetal interface. We aimed to map differentially expressed genes and pathways affected in case of RM. Affymetrix® GeneChip® HG-U133 Plus 2.0 Array was applied to placental tissue from 4 RM cases (mean gestational age 63 days) and 6 elective abortions as controls (mean gestational age 62.8 days). Between the two groups 30 transcripts representing 27 genes showed differential expression. 10 genes with the highest fold-change were chosen for validation and further replicated in an independent sample set (9 RM cases, 17 controls) using Taqman® RT-qPCR. RM patients exhibited significant upregulation of two genes: apoptosis inducing ligand TRAIL (p=1.4x10-3) and S100A8 (p=7.9x10-4), encoding for inflammatory marker calprotectin. Combinatory effect of TRAIL, S100A8 and ASMTL provided a highly sensitive test distinguishing RM cases from controls (ROC analysis, area under curve=0.967). Immunohistochemical staining detected TRAIL and ASMTL mainly in trophoblastic cells and S100A8 in myeloid cells of maternal blood at maternal-fetal interface of first trimester placenta. In conclusion, genome wide expression profiling distinguished three differentially expressed genes in RM placentas: TRAIL, S100A8 and ASMTL. Although the detected gene expression alterations related to various pathways could be primary (causing) or secondary (consequence) events associated with the process of RM, the joint contribution of identified markers may provide a highly predictive test for detection of early pregnancy complications 10 gene arrays, 6 in control group and 4 in cases

2010-12-31 | E-GEOD-22490 | biostudies-arrayexpress

Characterization of Gene Expression At the Human Maternal-Fetal Interface

Project description:Microarray analysis to globally assess gene expression at the maternal-fetal interface Keywords: age

2007-01-11 | GSE5999 | GEO