ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2021
Cytotrophoblasts suppress macrophage-mediated inflammation through a contact-dependent mechanism.
Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Decidua macrophages display a restrained inflammatory profile during chorioamnionitis.Frontiers in immunology · 2026Article
- Group B Streptococcal Membrane Vesicles Induce Proinflammatory Cytokine Production and Are Sensed in an NLRP3 Inflammasome-Dependent Mechanism in a Human Macrophage-like Cell Line.ACS infectious diseases · 2025Article
- Neu5Gc regulates decidual macrophages leading to abnormal embryo implantation.Genes and immunity · 2024Article
- Reproductive organ on-a-chip technologies and assessments of the fetal-maternal interface.Frontiers in lab on a chip technologies · 2024Article
- Palmitate and group BFrontiers in immunology · 2024Article
- TNF-α-positive patients with recurrent pregnancy loss: The etiology and management.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024Article
- Inhibition of lipopolysaccharide-induced inflammation by trophoblast-conditioned medium and trophoblast-derived extracellular vesicles in human middle ear epithelial cells.Scientific reports · 2023Article
- WD repeat domain 5 promotes the development of late-onset preeclampsia by activating nuclear factor kappa B.Acta cirurgica brasileira · 2023Article
- Group B Streptococcus: Virulence Factors and Pathogenic Mechanism.Microorganisms · 2022Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
problemGestational membrane (GM) infection provokes inflammation and can result in preterm prelabor rupture of membranes (PPROM). The choriodecidual layer of the GM includes decidual stromal cells (DSC), cytotrophoblasts (CTB), and macrophages (Mφ). Our laboratory has previously shown that DSCs suppress Mφ TNF-α production through secreted prostaglandin E METHOD OF STUDY: THP.1 Mφ-like cells with an NF-κB reporter construct or human blood monocyte-derived Mφ were co-cultured with the Jeg3 CTB cell line or primary human CTBs and challenged with group B streptococcus (GBS) or Toll-like receptor (TLR) agonists. Conditioned medium generated from CTB cultures was applied to Mφ cultures before infection or treatment. Alternatively, CTBs were co-incubated with, but physically separated from, Mφ and GBS or TLR-stimulated. NF-κB was assessed via alkaline phosphatase assay, and proinflammatory mediators were assessed by qRT-PCR and ELISA.
resultsCTBs suppressed GBS- or TLR-stimulated Mφ NF-κB activity, and TNF-α and MMP9 production. Direct physical contact between CTBs and Mφ was required for full immunosuppression. Immunosuppression could be overcome by increasing the ratio of Mφ to CTB.
conclusionsCTBs limit Mφ NF-κB activation and production of TNF-α and MMP9 through an as-yet unknown, cell-to-cell contact-mediated mechanism. This suppression is distinct from the PGE
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