IL-1 and TNF mediates IL-6 signaling at the maternal-fetal interface during intrauterine inflammation.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2024
Historique:
received: 11 04 2024
accepted: 20 05 2024
medline: 19 6 2024
pubmed: 19 6 2024
entrez: 19 6 2024
Statut: epublish

Résumé

IL6 signaling plays an important role in triggering labor and IL6 is an established biomarker of intrauterine infection/inflammation (IUI) driven preterm labor (PTL). The biology of IL6 during IUI at the maternal-fetal interface was investigated in samples from human subjects and non-human primates (NHP). Pregnant women with histologic chorioamnionitis diagnosed by placenta histology were recruited (n=28 term, n=43 for preterm pregnancies from 26-36 completed weeks of gestation). IUI was induced in Rhesus macaque by intraamniotic injection of lipopolysachharide (LPS, n=23). IL1 signaling was blocked using Anakinra (human IL-1 receptor antagonist, n=13), and Tumor necrosis factor (TNF) signaling was blocked by anti TNF-antibody (Adalimumab n=14). The blockers were given before LPS. All animals including controls (intraamniotic injection of saline n=27), were delivered 16h after LPS/saline exposure at about 80% gestation. IUI induced a robust expression of These data suggest that IL1 and TNF blockers may be useful anti-inflammatory agents via suppression of IL6 signaling at the maternal-fetal interface.

Identifiants

pubmed: 38895127
doi: 10.3389/fimmu.2024.1416162
pmc: PMC11183269
doi:

Substances chimiques

Interleukin-6 0
Tumor Necrosis Factor-alpha 0
Lipopolysaccharides 0
Interleukin-1 0
Interleukin 1 Receptor Antagonist Protein 0
IL6 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1416162

Informations de copyright

Copyright © 2024 Presicce, Roland, Senthamaraikannan, Cappelletti, Hammons, Miller, Jobe, Chougnet, DeFranco and Kallapur.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Pietro Presicce (P)

Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, CA, United States.

Cynthia Roland (C)

Department of Obstetrics/Gynecology, Maternal-Fetal Medicine, University of Cincinnati, Cincinnati, OH, United States.

Paranthaman Senthamaraikannan (P)

Division of Neonatology/Pulmonary Biology, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, Cincinnati, OH, United States.

Monica Cappelletti (M)

Division of Immunogenetics, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, CA, United States.

McKensie Hammons (M)

Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, CA, United States.

Lisa A Miller (LA)

Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis, Davis, CA, United States.

Alan H Jobe (AH)

Division of Neonatology/Pulmonary Biology, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, Cincinnati, OH, United States.

Claire A Chougnet (CA)

Immunobiology, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, Cincinnati, OH, United States.

Emily DeFranco (E)

Department of Obstetrics/Gynecology, Maternal-Fetal Medicine, University of Cincinnati, Cincinnati, OH, United States.

Suhas G Kallapur (SG)

Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, CA, United States.

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Classifications MeSH