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Decidual lymphatic endothelial cell-derived granulocyte-macrophage colony-stimulating factor induces M1 macrophage polarization via the NF-κB pathway in severe pre-eclampsia. | LitMetric

Decidual lymphatic endothelial cell-derived granulocyte-macrophage colony-stimulating factor induces M1 macrophage polarization via the NF-κB pathway in severe pre-eclampsia.

Am J Reprod Immunol

Department of Obstetrics and Gynecology, Institute of Women's Medical Life Science, Placenta-derived Stem Cell and Genomic Research Lab, Yonsei University College of Medicine, Yonsei University Health System, Seoul, The Republic of Korea.

Published: August 2023

AI Article Synopsis

  • The study investigates the interaction between decidual lymphatic endothelial cells (dLECs) and macrophages in the context of pre-eclampsia (PE), focusing on how dLECs influence macrophage polarization toward a proinflammatory M1 phenotype.
  • Researchers cocultured THP-1 macrophages with dLECs or their conditioned medium, measuring macrophage polarization and signaling pathways involved, notably the GM-CSF/NF-κB pathway.
  • Results show that PE dLECs increase M1 macrophage polarization by secreting GM-CSF, and this process is regulated by NF-κB activation, indicating a significant role of dLECs in the inflammatory response in PE.

Article Abstract

Problem: Direct interactions between macrophages and lymphatic vessels have been shown previously. In pre-eclampsia (PE), macrophages are dominantly polarized into a proinflammatory M1 phenotype and lymphangiogenesis is defective in the decidua. Here, we investigated whether decidual lymphatic endothelial cells (dLECs) affect macrophage polarization in PE.

Method Of Study: THP-1 macrophages were cocultured with dLECs or cultured in the conditioned medium (CM) of dLECs. Macrophage polarization was measured using flow cytometry. Granulocyte-macrophage colony-stimulating factor (GM-CSF) expression in dLECs was measured using qRT-PCR and ELISA. The activation of nuclear translocation of nuclear factor-κ (NF-κB), an upstream signaling molecule of GM-CSF, was assessed by immunocytochemical localization of p65. Through GM-CSF knockdown and NF-κB inhibition in dLEC, we evaluated whether the GM-CSF/NF-κB pathway of PE dLEC affects decidual macrophage polarization.

Results: The ratio of inflammatory M1 macrophages with HLA-DR /CD80 markers significantly increased following coculturing with PE dLECs or culturing in PE dLEC CM, indicating that the PE dLEC-derived soluble factor acts in a paracrine manner. GM-CSF expression was significantly upregulated in PE dLECs. Recombinant human GM-CSF induced macrophage polarization toward an M1-like phenotype, whereas its knockdown in PE dLECs suppressed it, suggesting PE dLECs induce M1 macrophage polarization by secreting GM-CSF. The NF-κB p65 significantly increased in PE dLECs compared to the control, and pretreatment with an NF-κB inhibitor significantly suppressed GM-CSF production from PE dLECs.

Conclusions: In PE, dLECs expressing high levels of GM-CSF via the NF-κB-dependent pathway play a role in inducing decidual M1 macrophage polarization.

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Source
http://dx.doi.org/10.1111/aji.13744DOI Listing

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