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Lipopolysaccharide-Stimulated Human Fetal Membranes Induce Neutrophil Activation and Release of Vital Neutrophil Extracellular Traps.脂多糖刺激的人胎膜诱导中性粒细胞活化并释放重要的中性粒细胞细胞外陷阱。
J Immunol. 2019 Jul 15;203(2):500-510. doi: 10.4049/jimmunol.1900262. Epub 2019 Jun 5.
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Viral Infection Sensitizes Human Fetal Membranes to Bacterial Lipopolysaccharide by MERTK Inhibition and Inflammasome Activation.病毒感染通过抑制MERTK和激活炎性小体使人类胎膜对细菌脂多糖敏感。
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Zika virus infection of Hofbauer cells.霍夫鲍尔细胞的寨卡病毒感染
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Zika virus productively infects primary human placenta-specific macrophages.寨卡病毒可有效感染原代人胎盘特异性巨噬细胞。
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Zika Virus Targets Different Primary Human Placental Cells, Suggesting Two Routes for Vertical Transmission.寨卡病毒靶向不同的原代人胎盘细胞，提示垂直传播的两条途径。
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Zika Virus Infects Human Placental Macrophages.寨卡病毒感染人胎盘巨噬细胞。
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Type I Interferon Regulates the Placental Inflammatory Response to Bacteria and is Targeted by Virus: Mechanism of Polymicrobial Infection-Induced Preterm Birth.I型干扰素调节胎盘对细菌的炎症反应并被病毒靶向：多微生物感染诱导早产的机制。
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Acute chorioamnionitis and funisitis: definition, pathologic features, and clinical significance.急性绒毛膜羊膜炎和脐带炎：定义、病理特征及临床意义。
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疱疹病毒感染的Hofbauer 细胞通过 IL-1β 依赖的机制激活血管内皮细胞。

Herpesvirus-infected Hofbauer cells activate endothelial cells through an IL-1β-dependent mechanism.

机构信息

Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, CT, USA.

Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, East Lansing, MI, USA.

出版信息

Placenta. 2020 Feb;91:59-65. doi: 10.1016/j.placenta.2020.01.010. Epub 2020 Jan 25.

DOI:10.1016/j.placenta.2020.01.010
PMID:32174308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7078070/
Abstract

INTRODUCTION

Placental 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.

METHODS

HBCs 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).

RESULTS

MHV-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.

摘要

简介

胎盘病毒感染与胎儿炎症和不良妊娠结局有关。然而，关于绒毛和相邻胎儿脐内皮细胞中的胎盘巨噬细胞如何对病毒刺激做出反应的研究有限。本研究旨在评估在病毒感染过程中豪夫鲍尔细胞（Hofbauer cells，HBCs）与脐静脉内皮细胞（human umbilical vein endothelial cells，HUVECs）之间的通讯。

方法

HBCs 未感染或感染γ疱疹病毒 MHV-68，并收集条件培养基（conditioned medium，CM）。将 HUVECs 暴露于 HBC CM 中，并通过 ELISA 和 qPCR 测量促中性粒细胞反应标志物：白细胞介素 8（IL-8）、E-选择素、细胞间黏附分子 1（intercellular adhesion molecule 1，ICAM-1）和血管细胞黏附分子 1（vascular adhesion molecule 1，VCAM-1）的水平。使用白细胞介素 1β 阻断抗体（Ab）或白细胞介素 1 受体拮抗剂（IL-1Ra）研究 HBC 衍生的白细胞介素 1β 的作用。

结果

MHV-68 感染 HBCs 可显著诱导白细胞介素 1β 的分泌。感染 HBC 的 CM 诱导 HUVEC 表达 IL-8、E-选择素、VCAM-1、ICAM-1mRNA 的表达，并诱导 IL-8 的分泌。中和白细胞介素 1β Ab 和白细胞介素 1Ra 可抑制 HUVEC 对 MHV 感染 HBC 的 CM 的反应。

讨论

病毒诱导的 HBC 白细胞介素 1β 激活 HUVEC 产生促中性粒细胞反应。这种新的细胞间通讯途径可能在与胎盘病毒感染相关的胎儿炎症的发生中起重要作用。

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