ArticleBiology of reproduction2016
Effects of Lipopolysaccharide on Human First Trimester Villous Cytotrophoblast Cell Function In Vitro.
Article in Biology of reproduction, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Association Between TLR4 Gene Polymorphisms and Risk of Preeclampsia: Systematic Review and Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021Pooled it
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- HMGB1 in depression: An overview of microglial HMBG1 in the pathogenesis of depression.Brain, behavior, & immunity - health · 2023Review
- Benzo(a)pyrene induced adverse pregnancy outcomes by affecting the expression of IL-18 and IL-1RN in placenta.Heliyon · 2022Article
- Testis-specific fascin component FSCN3 is dispensable for mouse spermatogenesis and fertility.Molecular biology reports · 2022Article
- Myometrial-derived CXCL12 promotes lipopolysaccharide induced preterm labour by regulating macrophage migration, polarization and function in mice.Journal of cellular and molecular medicine · 2022Article
- The relationship among vitamin D, TLR4 pathway and preeclampsia.Molecular biology reports · 2020Review
- Decidual CD8Journal of translational medicine · 2020Article
- Identification of microRNAs and their target genes in the placenta as biomarkers of inflammation.Clinical and experimental reproductive medicine · 2020Article
- Transcriptomic and functional analyses of 3D placental extravillous trophoblast spheroids.Scientific reports · 2019Article
- Analysis of the capacity of Salmonella enterica Typhimurium to infect the human Placenta.Placenta · 2019Article
- IL-1 receptor antagonist therapy mitigates placental dysfunction and perinatal injury following Zika virus infection.JCI insight · 2019Article
- Rosiglitazone blocks first trimester in-vitro placental injury caused by NF-κB-mediated inflammation.Scientific reports · 2019Article
- Lipopolysaccharide-induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Article
- Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory TInternational journal of biological sciences · 2017Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
It has been shown that adverse obstetrical outcomes such as pre-eclampsia and intrauterine growth retardation correlate with maternal infection. In this study, we investigated mechanisms involved in infection-associated abnormalities in cytotrophoblast function. Primary human first trimester cytotrophoblast cells were isolated and treated with lipopolysaccharide (LPS). Levels of the cytokines and chemokines were measured and cytotrophoblast invasion was investigated. In addition, first trimester decidual macrophages were isolated and treated with the conditioned medium from LPS-treated cytotrophoblast cells, and macrophage migration was assessed. Coculturing decidual macrophages with cytotrophoblast cells was conducted to investigate macrophage costimulatory molecule and receptor expression and intracellular cytokine production. We found that LPS exposure increased cytotrophoblast production of pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-6, and chemokines IL-8, macrophage inflammatory protein (MIP)-1alpha, and CXCL12 in a dose-dependent manner. In addition, LPS decreased cytotrophoblast invasion, and its effect was Toll-like receptor 4 (TLR4)-dependent and partly TNF-alpha-dependent. Conditioned medium from LPS-stimulated cytotrophoblast cells increased decidual macrophage migration and this effect was partly TLR4-dependent. Furthermore, coculturing decidual macrophages with LPS-exposed cytotrophoblast cells up-regulated macrophage CD80 and CD86 expression and intracellular TNF-alpha and IL-12p40 production, while down-regulating macrophage CD206 and CD209 expression and intracellular IL-10 secretion. LPS-stimulated macrophages also inhibited cytotrophoblast invasion. In conclusion, our results indicate that LPS increases the production of a subset of proinflammatory cytokines and chemokines by human first trimester cytotrophoblast cells, decreases cytotrophoblast invasion, and alters the cross talk between cytotrophoblast cells and decidual macrophages.
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