ArticleCellular & molecular immunology2021
Placenta-derived IL-32β activates neutrophils to promote preeclampsia development.
Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- CD81 restricts decidual IGF2-mediated smooth muscle cell dedifferentiation during spiral artery remodeling in preeclampsia.BMC medicine · 2026Article
- Ferroptosis-related gene BACH1 is associated with preeclampsia and shows potential as a biomarker.BMC pregnancy and childbirth · 2026Article
- Multimodal single-cell protein and RNA profiling unveils dysregulated immature neutrophil dynamics in gestational diabetes mellitus.Communications biology · 2026Article
- Causal effects of maternal BMI on pregnancy outcomes: a Mendelian randomisation study investigating the mediating role of blood counts.Frontiers in genetics · 2026Article
- IL-32 as a potential biomarker and therapeutic target in cardiovascular disease.Frontiers in immunology · 2026Review
- A single-cell cytokine dictionary of human peripheral blood.bioRxiv : the preprint server for biology · 2025Article
- A single-cell cytokine dictionary of human peripheral blood.Research square · 2025Article
- Evaluating the predictive value of systemic inflammation indices in early pregnancy loss: a retrospective observational study.BMC immunology · 2025Observational
- First-trimester pan-immune-inflammation value predicts preeclampsia in a dose-dependent linear pattern.BMC pregnancy and childbirth · 2025Article
- Article
- Multi-omics-based mapping of decidualization resistance in patients with a history of severe preeclampsia.Nature medicine · 2025Article
- Interleukin-32: a Pandora's box in human immunodeficiency virus infection.Frontiers in immunology · 2025Review
- Targeting Neutrophil Extracellular Trap Formation: Exploring Promising Pharmacological Strategies for the Treatment of Preeclampsia.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Unveiling sialoglycans' immune mastery in pregnancy and their intersection with tumor biology.Frontiers in immunology · 2024Review
- Basic Research Advances in China on Embryo Implantation, Placentation, and Parturition.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2024Article
- Extracellular Vesicles Derived from Human Umbilical Cord MSC Improve Vascular Endothelial Function in In Vitro and In Vivo Models of Preeclampsia through Activating Arginine Metabolism.Molecular pharmaceutics · 2023Article
- Obesity Correlates with Chronic Inflammation of the Innate Immune System in Preeclampsia and HELLP Syndrome during Pregnancy.Biomedicines · 2023Article
- IL-32-driven neutrophil activation in preeclampsia.Cellular & molecular immunology · 2023Article
- Targeting endometrial inflammation in intrauterine adhesion ameliorates endometrial fibrosis by priming MSCs to secrete C1INH.iScience · 2023Article
- Circulating Interlukin-32 and Altered Blood Pressure Control in Individuals with Metabolic Dysfunction.International journal of molecular sciences · 2023Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune activation at the maternal-fetal interface is a main pathogenic factor of preeclampsia (PE). Neutrophils (PMNs) are activated in PE patients, but the mechanism and consequences of PMN activation need to be further explored. Here, we demonstrated that interleukin-32 (IL-32) expression was significantly upregulated in syncytiotrophoblasts (STBs) and that IL-32β was the major isoform with increased expression in the placenta of severe PE (sPE) patients. Furthermore, the level of IL-32 expression in the placenta was correlated with its level in the serum of sPE patients, indicating that IL-32 in the serum is derived mainly from the placenta. Then, in vitro experiments showed that IL-32β could highly activate PMNs and that these IL-32β-activated PMNs were better able to adhere to endothelial cells (HUVECs) and enhance the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) in HUVECs, which could be reversed by preincubation with the NADPH oxidase inhibitor VAS 2870. In addition, we showed that IL-32β mainly activated PMNs by binding to proteinase 3. Finally, IL-32β administration induced a PE-like phenotype in a pregnant mouse model. This study provides evidence of the involvement of IL-32β in the pathogenesis of PE.
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