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Predictive biomarkers and maternal immune alterations in postpartum preeclampsia reveal an immune-driven pathology

ABSTRACT: Predictive biomarkers and maternal immune alterations in postpartum preeclampsia reveal an immune-driven pathology

PROVIDER: PRJNA1093097 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28491758_1.fastq.gz	Fastqsanger.gz
	SRR28491758_2.fastq.gz	Fastqsanger.gz
	SRR28491759_1.fastq.gz	Fastqsanger.gz
	SRR28491759_2.fastq.gz	Fastqsanger.gz
	SRR28491760_1.fastq.gz	Fastqsanger.gz

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Predictive biomarkers and maternal immune alterations in postpartum preeclampsia reveal an immune-driven pathology

Project description:Postpartum preeclampsia (PPPE) is an under-diagnosed condition, developing within 48 hours to 6 weeks following an uncomplicated pregnancy. The etiology of PPPE is still unknown, leaving patients vulnerable and making the identification and treatment of patients requiring postpartum care an unmet need. We aimed to understand the immune contribution to PPPE at the time of diagnosis, as well as uncover the predictive potential of perinatal biomarkers for the early postnatal identification of high-risk patients. Placentas were collected at delivery from uncomplicated pregnancies (CTL) and PPPE patients for immunohistochemistry analysis. In this initial study, blood samples in PPPE patients were collected at the time of PPPE diagnosis (48h-25 days postpartum; mean 7.4 days) and compared to CTL blood samples taken 24h after delivery. Single-cell transcriptomics, flow cytometry, intracellular cytokine staining, and the circulating levels of inflammatory mediators were evaluated in the blood. Placental CD163+ cells and 1st trimester blood pressures can be valuable non-invasive and predictive biomarkers of PPPE with strong clinical application prospects. Furthermore, changes in immune cell populations, as well as cytokine production by CD14+, CD4+, and CD8+ cells, suggested a dampened response with an exhausted phenotype including decreased IL1b, IL12, and IFNg as well as elevated IL10. Understanding maternal immune changes at the time of diagnosis and prenatally within the placenta in our sizable cohort will serve as groundwork for pre-clinical and clinical research, as well as guiding clinical practice for example in the development of immune-targeted therapies, and early postnatal identification of patients who would benefit from more thorough follow-ups and risk education in the weeks following an uncomplicated pregnancy.

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Project description:Preeclampsia (PE) is characterized by sustained hypertension and proteinuria at a gestational age of 20 weeks or more. Immune system alterations are associated with the origin and the pathophysiology of preeclampsia, however, little is known about the landscape and heterogeneity of maternal immune system at the single-cell level. In this study, we performed single-cell RNA sequencing of 80,429 cells in PE patients and health controls, including T cells, B cells, natural killer (NK) cells, myeloid cells in peripheral blood mononuclear cells to characterize the immune cell subgroups at the pregnant and postpartum stages of PE. Our work showed that there was excessive activation of B cells, monocytes and NK cells in PE patients at the pregnant stage. Additionally, lower immune response activation was noticed in CD4+ and CD8+ T cells in PEs, especially the low-activation of memory T cells at the pregnant and postpartum stages. Moreover, there was a higher activation of B cells in pregnancy persisted postpartum in PEs, together with lower activation of memory T cells. These indicated their persistent effects on PE and its recurrence risks.

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Placental Immune alterations in early-onset preeclampsia and late-onset preeclampsia

Project description:Preeclampsia is a severe placenta-related pregnancy disorder that is generally divided into two subtypes named early-onset preeclampsia (onset <34 weeks of gestation), and lateonset preeclampsia (onset ≥34 weeks of gestation), with distinct pathophysiological origins. Both forms of preeclampsia have been associated with maternal systemic inflammation. However, alterations in the placental immune system have been less well characterized. Here, we studied immunological alterations in early- and late-onset preeclampsia placentas using a targeted expression profile approach. RNA was extracted from snap-frozen placenta samples (healthy n=13, early-onset preeclampsia n=13, and late-onset preeclampsia n=6). The expression of 730 immune-related genes from the Pan Cancer Immune Profiling Panel was measured, and the data were analyzed Q10 in the advanced analysis module of nSolver software (NanoString Technology). The results showed that early-onset preeclampsia placentas displayed reduced expression of complement, and toll-like receptor (TLR) associated genes, specifically TLR1 and TLR4. Mast cells and M2 macrophages were also decreased in early-onset preeclampsia compared to healthy pl acentas. The findings were confirmed by an immunohistochemistry approach using 20 healthy, 19 early-onset preeclampsia, and 10 late-onset preeclampsia placentas. We conclude that the placental innate immune system is altered in early-onset preeclampsia compared to uncomplicated pregnancies. The absence of these alterations in late-onset preeclampsia placentas indicates dissimilar immunological profiles. The study revealed distinct pathophysiological processes in earlyonset and late-onset preeclampsia placentas and imply that a tailored treatment to each subtype is desirable.

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Gene Expression Profiles Predict Postpartum-onset Depression Patients with Treatment-Resistant Depression Patients with Treatment-Resistant Depression

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Dual specificity phosphate 1 (DUSP1) has a key non-invasive predictive marker in preeclampsia

Project description:Dual specificity phosphate 1 (DUSP1) has a key non-invasive predictive marker in preeclampsia

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