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Searching for the influencers among placental immune cells in preeclampsia.

ABSTRACT: It has been posited that cells of the maternal and fetal immune systems communicate to lead to immune tolerance during pregnancy however been inconclusive. Here, we profiled single-cell transcriptional signatures by placental layers consisting of maternal-fetal interface (MF) and deep-placenta (Pla) regions, then searched influencer gene for preeclampsia (PE). As underpin principle of the failure of immune tolerance, we start by clarifying the systemic framework, which consists of immune interactions frequency (IIF) and specific trigger (i.e., influencer) tolerance (IT) models. We elaborate single-cell transcriptional profiles of normal term (Norm) and preeclampsia preterm parturitions (PePT). Fetal and maternal cells admixed across placenta, in both of Norms and PePTs, rejecting IIF model of immune failure of pregnancy posed by exceed interactions of fetomaternal cells. Whereases placental layers are well mixed with maternal cells, we identified conserved gradual immune transition of fetal T cells in both of PePT and Norm, disapproving IIF model. To search the influencer of PePT in IT model, we established and validated a classification model for PePT and Norm immune cells including T cells, then prioritized major contributors for classifier model. Interestingly, those prioritized genes are highly enriched with ligands and receptors (p-value 5.98e-05). Out of prioritized ligand-receptors, SPP1 and CD44 suggested as influencer of inflammation signatures and experimentally validated by exclusive colocalization of SPP1 and CD44 expressed cells in placentas of PePT. Different IL4 and IFN-g levels in the serum and urine of PePTs further support contribution of SPP1 in associated pathways, including allograft rjection pathway. Collectively, our finding provide insight into the influence of specific immune interactions between cells in human placenta and these influencer-derived impact the immune harmonization of PePT.

ORGANISM(S): Homo sapiens

PROVIDER: GSE290578 | GEO | 2025/05/26

REPOSITORIES: GEO

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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.

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Searching for the influencers among placental immune cells in preeclampsia.

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