ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Activation of the nuclear factor-κB pathway during postnatal lung inflammation preserves alveolarization by suppressing macrophage inflammatory protein-2.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 42 citations in OpenAlex.
- Mesenchyme-derived inflammation during the saccular stage recruits macrophages and alters lung development.JCI insight · 2026Article
- Clinical Interventions and Inflammatory Signaling Shape the Transcriptional and Cellular Architecture of the Early Postnatal Lung.bioRxiv : the preprint server for biology · 2025Article
- Research progress of microvascular development in bronchopulmonary dysplasia.Pediatric investigation · 2024Review
- Caffeine: The Story beyond Oxygen-Induced Lung and Brain Injury in Neonatal Animal Models-A Narrative Review.Antioxidants (Basel, Switzerland) · 2024Review
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- Losartan as a Reproposing Therapeutic Agent in Acute Respiratory Distress Syndrome: Modulating Inflammatory Responses and Cytokine Production.International journal of molecular and cellular medicine · 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
- Developmental diversity and unique sensitivity to injury of lung endothelial subtypes during postnatal growth.iScience · 2023Article
- TRAIL protects the immature lung from hyperoxic injury.Cell death & disease · 2022Article
- When inflammation meets lung development-an update on the pathogenesis of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2022Review
- Adrenomedullin Deficiency Potentiates Lipopolysaccharide-Induced Experimental Bronchopulmonary Dysplasia in Neonatal Mice.The American journal of pathology · 2021Article
- Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency.Cell and tissue research · 2021Article
- Effect of the Notch4/Dll4 signaling pathway in early gestational intrauterine infection on lung development.Experimental and therapeutic medicine · 2021Article
- Transforming Growth Factor-induced Protein Promotes NF-κB-mediated Angiogenesis during Postnatal Lung Development.American journal of respiratory cell and molecular biology · 2021Article
- MSC Based Therapies to Prevent or Treat BPD-A Narrative Review on Advances and Ongoing Challenges.International journal of molecular sciences · 2021Review
- SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia.Frontiers in medicine · 2021Review
- Single-Cell Analysis of the Neonatal Immune System Across the Gestational Age Continuum.Frontiers in immunology · 2021Article
- Interactive and independent effects of early lipopolysaccharide and hyperoxia exposure on developing murine lungs.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Phenotypes of Bronchopulmonary Dysplasia.International journal of molecular sciences · 2020Review
- Bacterial Colonization within the First Six Weeks of Life and Pulmonary Outcome in Preterm Infants <1000 g.Journal of clinical medicine · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
A significant portion of lung development is completed postnatally during alveolarization, rendering the immature lung vulnerable to inflammatory stimuli that can disrupt lung structure and function. Although the NF-κB pathway has well-recognized pro-inflammatory functions, novel anti-inflammatory and developmental roles for NF-κB have recently been described. Thus, to determine how NF-κB modulates alveolarization during inflammation, we exposed postnatal day 6 mice to vehicle (PBS), systemic lipopolysaccharide (LPS), or the combination of LPS and the global NF-κB pathway inhibitor BAY 11-7082 (LPS + BAY). LPS impaired alveolarization, decreased lung cell proliferation, and reduced epithelial growth factor expression. BAY exaggerated these detrimental effects of LPS, further suppressing proliferation and disrupting pulmonary angiogenesis, an essential component of alveolarization. The more severe pathology induced by LPS + BAY was associated with marked increases in lung and plasma levels of macrophage inflammatory protein-2 (MIP-2). Experiments using primary neonatal pulmonary endothelial cells (PEC) demonstrated that MIP-2 directly impaired neonatal PEC migration in vitro; and neutralization of MIP-2 in vivo preserved lung cell proliferation and pulmonary angiogenesis and prevented the more severe alveolar disruption induced by the combined treatment of LPS + BAY. Taken together, these studies demonstrate a key anti-inflammatory function of the NF-κB pathway in the early alveolar lung that functions to mitigate the detrimental effects of inflammation on pulmonary angiogenesis and alveolarization. Furthermore, these data suggest that neutralization of MIP-2 may represent a novel therapeutic target that could be beneficial in preserving lung growth in premature infants exposed to inflammatory stress.
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