ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Intra-amniotic IL-1β induces fetal inflammation in rhesus monkeys and alters the regulatory T cell/IL-17 balance.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 73 citations in OpenAlex.
- Evidence for Maternal Autoantibodies in the Pathogenesis of Preterm Birth.medRxiv : the preprint server for health sciences · 2025Article
- Ascending Vaginal Infection in Mice Induces Preterm Birth and Neonatal Morbidity.The American journal of pathology · 2025Article
- Systemic inflammatory responses to repeated and increasing endotoxin challenges in fetal sheep.Physiological reports · 2025Article
- IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.Cell communication and signaling : CCS · 2025Article
- Th17/Treg Cell Imbalance May Contribute to Spontaneous Preterm Labor.Journal of immunology research · 2025Review
- IL-1 and TNF mediates IL-6 signaling at the maternal-fetal interface during intrauterine inflammation.Frontiers in immunology · 2024Article
- Differential expression and localization of immunity-related factors in main immune organs of yak.Animal biotechnology · 2023Article
- c-Myc Drives inflammation of the maternal-fetal interface, and neonatal lung remodeling induced by intra-amniotic inflammation.Frontiers in cell and developmental biology · 2023Article
- The Expression of IL-1β Correlates with the Expression of Galectin-3 in the Tissue at the Maternal-Fetal Interface during the Term and Preterm Labor.Journal of clinical medicine · 2022Article
- Review
- Actions of Bisphenol A on Different Feto-Maternal Compartments Contributing to Preterm Birth.International journal of molecular sciences · 2022Review
- Maternal COVID-19 leaves a lasting immunological impression on the fetus.Nature immunology · 2021Article
- The induction of preterm labor in rhesus macaques is determined by the strength of immune response to intrauterine infection.PLoS biology · 2021Article
- Understanding Host-Pathogen Interactions in Acute Chorioamnionitis Through the Use of Animal Models.Frontiers in cellular and infection microbiology · 2021Review
- The fetal inflammatory response syndrome: the origins of a concept, pathophysiology, diagnosis, and obstetrical implications.Seminars in fetal & neonatal medicine · 2020Article
- Impact of ferumoxytol magnetic resonance imaging on the rhesus macaque maternal-fetal interface†.Biology of reproduction · 2020Article
- Pulmonary Consequences of Prenatal Inflammatory Exposures: Clinical Perspective and Review of Basic Immunological Mechanisms.Frontiers in immunology · 2020Review
- MHC II-PIFrontiers in immunology · 2020Article
- Maternal-Fetal Inflammation in the Placenta and the Developmental Origins of Health and Disease.Frontiers in immunology · 2020Review
- Histological Chorioamnionitis Induces Differential Gene Expression in Human Cord Blood Mononuclear Leukocytes from Term Neonates.Scientific reports · 2019Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Very low birth weight preterm newborns are susceptible to the development of debilitating inflammatory diseases, many of which are associated with chorioamnionitis. To define the effects of chorioamnionitis on the fetal immune system, IL-1β was administered intra-amniotically at ~80% gestation in rhesus monkeys. IL-1β caused histological chorioamnionitis, as well as lung inflammation (infiltration of neutrophils or monocytes in the fetal airways). There were large increases in multiple proinflammatory cytokine mRNAs in the lungs at 24 h postadministration, which remained elevated relative to controls at 72 h. Intra-amniotic IL-1β also induced the sustained expression of the surfactant proteins in the lungs. Importantly, IL-1β significantly altered the balance between inflammatory and regulatory T cells. Twenty-four hours after IL-1β injection, the frequency of CD3(+)CD4(+)FOXP3(+) T cells was decreased in lymphoid organs. In contrast, IL-17A-producing cells (CD3(+)CD4(+), CD3(+)CD4(-), and CD3(-)CD4(-) subsets) were increased in lymphoid organs. The frequency of IFN-γ-expressing cells did not change. In this model of a single exposure to an inflammatory trigger, CD3(+)CD4(+)FOXP3(+) cells rebounded quickly, and their frequency was increased at 72 h compared with controls. IL-17 expression was also transient. Interestingly, the T cell profile alteration was confined to the lymphoid organs and not to circulating fetal T cells. Together, these results suggest that the chorioamnionitis-induced IL-1/IL-17 axis is involved in the severe inflammation that can develop in preterm newborns. Boosting regulatory T cells and/or controlling IL-17 may provide a means to ameliorate these abnormalities.
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