Herpesvirus-infected Hofbauer cells activate endothelial cells through an IL-1β-dependent mechanism.
FIRS
Herpesvirus
Hofbauer cells
IL-1β
Macrophages
Placenta
Journal
Placenta
ISSN: 1532-3102
Titre abrégé: Placenta
Pays: Netherlands
ID NLM: 8006349
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
25
10
2019
revised:
10
12
2019
accepted:
22
01
2020
entrez:
17
3
2020
pubmed:
17
3
2020
medline:
9
2
2021
Statut:
ppublish
Résumé
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. 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). 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. 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.
Identifiants
pubmed: 32174308
pii: S0143-4004(20)30020-5
doi: 10.1016/j.placenta.2020.01.010
pmc: PMC7078070
mid: NIHMS1553285
pii:
doi:
Substances chimiques
IL1B protein, human
0
Interleukin-1beta
0
Vascular Cell Adhesion Molecule-1
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
59-65Subventions
Organisme : NICHD NIH HHS
ID : P01 HD054713
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI131613
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest None.
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