ArticlePlacenta2020
Herpesvirus-infected Hofbauer cells activate endothelial cells through an IL-1β-dependent mechanism.
Article in Placenta, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis.International journal of molecular sciences · 2023Article
- Monocytes from Uninfected Neonates Born toPathogens (Basel, Switzerland) · 2023Article
- Pregnancy-Specific Glycoprotein 9 Enhances Store-Operated Calcium Entry and Nitric Oxide Release in Human Umbilical Vein Endothelial Cells.Diagnostics (Basel, Switzerland) · 2023Article
- Placental macrophage responses to viral and bacterial ligands and the influence of fetal sex.iScience · 2022Article
- Article
- Innate immune defenses at the maternal-fetal interface.Current opinion in immunology · 2022Review
- Congenital Infection Influence on Early Brain Development Through the Gut-Brain Axis.Frontiers in neuroscience · 2022Review
- Article
- Placental Macrophage (Hofbauer Cell) Responses to Infection During Pregnancy: A Systematic Scoping Review.Frontiers in immunology · 2021Article
- NLRP3 inflammasome function and pyroptotic cell death in human placental Hofbauer cells.Journal of reproductive immunology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
introductionPlacental viral infections are associated with fetal inflammation and adverse pregnancy outcomes. However, there have been limited studies on how placental macrophages in the villous and adjacent fetal umbilical endothelial cells respond to a viral insult. This study aimed to evaluate the communication between Hofbauer cells (HBCs) and human umbilical vein endothelial cells (HUVECs) during a viral infection.
methodsHBCs were either uninfected or infected with the γ-herpesvirus, MHV-68, and the conditioned medium (CM) collected. HUVECs were exposed to HBC CM and the levels of the pro-neutrophilic response markers: IL-8; E-selectin; intercellular adhesion molecule 1 (ICAM-1); and vascular adhesion molecule 1 (VCAM-1) measured by ELISA and qPCR. The role of HBC-derived IL-1β was investigated using an IL-1β blocking antibody (Ab) or IL-1 receptor antagonist (IL-1Ra).
resultsMHV-68 infection of HBCs induced a significant increase in IL-1β secretion. CM from infected HBCs induced HUVEC expression of IL-8, E-selectin, VCAM-1, ICAM-1 mRNA, and secretion of IL-8. The HUVEC response to the CM of MHV-infected HBCs was inhibited by a neutralizing IL-1β Ab and by IL-1Ra. DISCUSSION: Virally-induced HBC IL-1β activates HUVECs to generate a pro-neutrophilic response. This novel cell-cell communication pathway may play an important role in the genesis of fetal inflammation associated with placental viral infection.
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