ArticleJournal of immunology (Baltimore, Md. : 1950)2016
IL-1β and Inflammasome Activity Link Inflammation to Abnormal Fetal Airway Development.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
- Mesenchyme-derived inflammation during the saccular stage recruits macrophages and alters lung development.JCI insight · 2026Article
- Bronchopulmonary Dysplasia and Innate Immunity: A Narrative Review of the Roles of IL-1β and IL-8 (CXCL8).Children (Basel, Switzerland) · 2026Review
- Proinflammatory monocyte-derived granulocyte-macrophage colony-stimulating factor fuels airway inflammation in bronchopulmonary dysplasia.Pediatric research · 2026Article
- Pulmonary organoid models demonstrate compositionally driven epithelial plasticity and immune polarization.iScience · 2026Article
- Levels of IL-1β and IL-1 receptor antagonist (IL-1Ra) in Moroccan children admitted to the pediatric emergency department for febrile seizures.BMC pediatrics · 2026Article
- Spontaneous Pregravid Obesity Reshapes Fetal Immune Ontogeny in a Nonhuman Primate Model.bioRxiv : the preprint server for biology · 2026Article
- PKM2 Promotes Glycolysis in Alveolar Macrophages and Induces Inflammation in Bronchopulmonary Dysplasia.Inflammation · 2026Article
- Transcriptional coordination in multicellular lineage differentiation during lung organogenesis: deciphering the role of epithelial cells as a microenvironmental regulatory hub.Frontiers in cell and developmental biology · 2026Review
- Review
- Ascending Vaginal Infection in Mice Induces Preterm Birth and Neonatal Morbidity.The American journal of pathology · 2025Article
- Fetal origin of bronchopulmonary dysplasia: contribution of intrauterine inflammation.Molecular medicine (Cambridge, Mass.) · 2024Review
- Fetal hypoplastic lungs have multilineage inflammation that is reversed by amniotic fluid stem cell extracellular vesicle treatment.Science advances · 2024Article
- Myeloid Nrf2 Protects against Neonatal Oxidant-Stress-Induced Lung Inflammation and Alveolar Simplification in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Mechanistic Approach on the Pulmonary Oxido-Inflammatory Stress Induced by Cobalt Ferrite Nanoparticles in Rats.Biological trace element research · 2024Article
- Early human lung immune cell development and its role in epithelial cell fate.Science immunology · 2023Article
- A key role for NLRP3 signaling in preterm labor and birth driven by the alarmin S100B.Translational research : the journal of laboratory and clinical medicine · 2023Article
- Sp3 is essential for normal lung morphogenesis and cell cycle progression during mouse embryonic development.Development (Cambridge, England) · 2023Article
- The Impact of Curcumin on Immune Response: An Immunomodulatory Strategy to Treat Sepsis.International journal of molecular sciences · 2022Review
- Establishment of tissue-resident immune populations in the fetus.Seminars in immunopathology · 2022Review
- Insights into the Black Box of Intra-Amniotic Infection and Its Impact on the Premature Lung: From Clinical and Preclinical Perspectives.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation in the developing preterm lung leads to disrupted airway morphogenesis and chronic lung disease in human neonates. However, the molecular mechanisms linking inflammation and the pathways controlling airway morphogenesis remain unclear. In this article, we show that IL-1β released by activated fetal lung macrophages is the key inflammatory mediator that disrupts airway morphogenesis. In mouse lung explants, blocking IL-1β expression, posttranslational processing, and signaling protected the formation of new airways from the inhibitory effects ofEscherichia coliLPS. Consistent with a critical role for IL-1β, mice expressing a gain-of-functionNlrp3allele and subsequent overactive inflammasome activity displayed abnormal saccular-stage lung morphogenesis and died soon after birth. Although the early-stage fetal lung appeared capable of mounting an NF-κB-mediated immune response, airway formation became more sensitive to inflammation later in development. This period of susceptibility coincided with higher expression of multiple inflammasome components that could increase the ability to release bioactive IL-1β. Macrophages fromNlrp3gain-of-function mice also expressed higher levels of more mature cell surface markers, additionally linking inflammasome activation with macrophage maturation. These data identify developmental expression of the inflammasome and IL-1β release by fetal lung macrophages as key mechanisms and potential therapeutic targets for neonatal lung disease.
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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 OpenQuestion graph.