IL-1 and TNF mediates IL-6 signaling at the maternal-fetal interface during intrauterine inflammation.
Female
Pregnancy
Humans
Animals
Interleukin-6
/ metabolism
Signal Transduction
Macaca mulatta
Tumor Necrosis Factor-alpha
/ metabolism
Chorioamnionitis
/ immunology
Lipopolysaccharides
/ immunology
Interleukin-1
/ metabolism
Adult
Obstetric Labor, Premature
/ immunology
Inflammation
/ immunology
Interleukin 1 Receptor Antagonist Protein
/ metabolism
Placenta
/ metabolism
amnion
chorioamnionitis
inflammation
innate immunity
reproductive immunology
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2024
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
1416162Informations 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.