ArticleMucosal immunology2022
A potent myeloid response is rapidly activated in the lungs of premature Rhesus macaques exposed to intra-uterine inflammation.
Article in Mucosal immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 6 citations in OpenAlex.
- Mesenchyme-derived inflammation during the saccular stage recruits macrophages and alters lung development.JCI insight · 2026Article
- Multi-omics insights into immune tolerance at the maternal-fetal interface in recurrent pregnancy loss: mechanisms, integration challenges, and translational perspectives.Frontiers in immunology · 2026Review
- Prenatal Melatonin Therapy Enhances Postnatal Lung Development in a Mouse Model of Inflammation-Induced Preterm Birth.Antioxidants (Basel, Switzerland) · 2025Article
- Pulmonary and neurobehavioral efficacies of AVR-48, a TLR4 modulator, in a preterm lamb model of bronchopulmonary dysplasia.Respiratory research · 2025Article
- Impact of intraamniotic inflammation on tryptophan metabolism in the placenta-fetal brain axis in rats.Reproduction (Cambridge, England) · 2025Article
- Fetal origin of bronchopulmonary dysplasia: contribution of intrauterine inflammation.Molecular medicine (Cambridge, Mass.) · 2024Review
- IL-1 and TNF mediates IL-6 signaling at the maternal-fetal interface during intrauterine inflammation.Frontiers in immunology · 2024Article
- Amnion responses to intrauterine inflammation and effects of inhibition of TNF signaling in preterm Rhesus macaque.iScience · 2023Article
- Inflammatory blockade prevents injury to the developing pulmonary gas exchange surface in preterm primates.Science translational medicine · 2022Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 3 countries.
Funding
Abstract
Up to 40% of preterm births are associated with histological chorioamnionitis (HCA), which leads to elevated levels of pro-inflammatory mediators and microbial products in the amniotic fluid, which come in contact with fetal lungs. Yet, fetal pulmonary immune responses to such exposure remain poorly characterized. To address this gap, we used our established HCA model, in which pregnant Rhesus macaques receive intraamniotic (IA) saline or LPS. IA LPS induced a potent and rapid myeloid cell response in fetal lungs, dominated by neutrophils and monocytes/macrophages. Infiltrating and resident myeloid cells exhibited transcriptional profiles consistent with exposure to TLR ligands, as well as cytokines, notably IL-1 and TNFα. Although simultaneous, in vivo blockade of IL-1 and TNFα signaling did not prevent the inflammatory cell recruitment, it blunted the lung overall inflammatory state reducing communication between, and activation of, infiltrating immune cells. Our data indicate that the fetal innate immune system can mount a rapid multi-faceted pulmonary immune response to in utero exposure to inflammation. These data provide mechanistic insights into the association between HCA and the postnatal lung morbidities of the premature infant and highlight therapeutic potential of inflammatory blockade in the fetus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.