ArticleAmerican journal of respiratory and critical care medicine2007
Nuclear factor-kappaB activation in neonatal mouse lung protects against lipopolysaccharide-induced inflammation.
Article in American journal of respiratory and critical care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
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- Yes-associated Protein Induces Age-dependent Inflammatory Signaling in the Pulmonary Endothelium.bioRxiv : the preprint server for biology · 2025Article
- Absence of IκBβ/NFκB signaling does not attenuate acetaminophen-induced hepatic injury.Anatomical record (Hoboken, N.J. : 2007) · 2025Article
- Effect and mechanism of transient receptor potential canonical channel 3 on hyperoxic lung injury in neonatal rats.Pediatric discovery · 2024Article
- Endothelial-specific loss of IKKβ disrupts pulmonary endothelial angiogenesis and impairs postnatal lung growth.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Stem/Progenitor Cells and Related Therapy in Bronchopulmonary Dysplasia.International journal of molecular sciences · 2023Review
- Dam-Infant Rhesus Macaque Pairs to Dissect Age-Dependent Responses to SARS-CoV-2 Infection.ImmunoHorizons · 2022Article
- Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency.Cell and tissue research · 2021Article
- Early Changes and Indicators Characterizing Lung Aging in Neonatal Chronic Lung Disease.Frontiers in medicine · 2021Review
- P2X7 Receptor Induces Pyroptotic Inflammation and Cartilage Degradation in Osteoarthritis via NF-Oxidative medicine and cellular longevity · 2021Article
- A Review of Placenta and Umbilical Cord-Derived Stem Cells and the Immunomodulatory Basis of Their Therapeutic Potential in Bronchopulmonary Dysplasia.Frontiers in pediatrics · 2021Review
- IL-1 promotes α-epithelial Sodium Channel (α-ENaC) expression in murine lung epithelial cells: involvement of NF-κB.Journal of cell communication and signaling · 2020Article
- Understanding the age divide in COVID-19: why are children overwhelmingly spared?American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Hyperoxia Injury in the Developing Lung Is Mediated by Mesenchymal Expression of Wnt5A.American journal of respiratory and critical care medicine · 2020Article
- Partial liquid ventilation-induced mild hypothermia improves the lung function and alleviates the inflammatory response during acute respiratory distress syndrome in canines.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2019Article
- Sex-differences in LPS-induced neonatal lung injury.Scientific reports · 2019Article
- Developmentally Regulated Innate Immune NFκB Signaling Mediates IL-1α Expression in the Perinatal Murine Lung.Frontiers in immunology · 2019Article
- Consequences of early postnatal lipopolysaccharide exposure on developing lungs in mice.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Intrauterine growth restriction decreases NF-κB signaling in fetal pulmonary artery endothelial cells of fetal sheep.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Distinct roles for IκB kinases alpha and beta in regulating pulmonary endothelial angiogenic function during late lung development.Journal of cellular and molecular medicine · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleInjurious agents often cause less severe injury in neonates as compared with adults.
objectiveWe hypothesized that maturational differences in lung inflammation induced by lipopolysaccharide (LPS) may be related to the nature of the nuclear factor (NF)-kappaB complex activated, and the profile of target genes expressed.
methodsNeonatal and adult mice were injected with intraperitoneal LPS. Lung inflammation was assessed by histology, and apoptosis was determined by TUNEL (terminal deoxynucleotidyl transferase UTP nick-end labeling). The expression of candidate inflammatory and apoptotic mediators was evaluated by quantitative real-time polymerase chain reaction and Western immunoblot.
resultsNeonates demonstrated reduced inflammation and apoptosis, 24 hours after LPS exposure, as compared with adults. This difference was associated with persistent activation of NF-kappaB p65p50 heterodimers in the neonates in contrast to early, transient activation of p65p50 followed by sustained activation of p50p50 in the adults. Adults had increased expression of a panel of inflammatory and proapoptotic genes, and repression of antiapoptotic targets, whereas no significant changes in these mediators were observed in the neonates. Inhibition of NF-kappaB activity in the neonates decreased apoptosis, but heightened inflammation, with increased expression of the same inflammatory genes elevated in the adults. In contrast, inhibition of NF-kappaB in the adults resulted in partial suppression of the inflammatory response.
conclusionsNF-kappaB activation in the neonatal lung is antiinflammatory, protecting against LPS-mediated lung inflammation by repressing similar inflammatory genes induced in the adult.
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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.