ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Myeloid-epithelial cross talk coordinates synthesis of the tissue-protective cytokine leukemia inhibitory factor during pneumonia.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting ICAM1 through LIF-mediated NF-κB/JAK2-STAT3 crosstalk protects nucleus pulposus from IL-1β-driven pyroptosis to ameliorate intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2025Article
- Transpulmonary LOX-1 Levels Are Predictive of Acute Respiratory Distress Syndrome After Cardiac Surgery: A Proof-of-Concept Study.Biomedicines · 2025Article
- Impact of treatment intensity on infectious complications in patients with acute myeloid leukemia.Journal of cancer research and clinical oncology · 2023Article
- The dysregulation of leukemia inhibitory factor and its implications for endometriosis pathophysiology.Frontiers in immunology · 2023Article
- Lectin-like oxidized low-density lipoprotein receptor 1 attenuates pneumonia-induced lung injury.JCI insight · 2022Article
- New Insights into the Alveolar Epithelium as a Driver of Acute Respiratory Distress Syndrome.Biomolecules · 2022Review
- Epithelial LIF signaling limits apoptosis and lung injury during bacterial pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Large scale cytokine profiling uncovers elevated IL12-p70 and IL-17A in severe pediatric acute respiratory distress syndrome.Scientific reports · 2021Article
- The emerging role of leukemia inhibitory factor in cancer and therapy.Pharmacology & therapeutics · 2021Review
- Neutrophil-Derived Oncostatin M Triggers Diverse Signaling Pathways during Pneumonia.Infection and immunity · 2021Article
- Combination Treatment With Remdesivir and Ivermectin Exerts Highly Synergistic and Potent Antiviral Activity Against Murine Coronavirus Infection.Frontiers in cellular and infection microbiology · 2021Article
- Novel therapeutic approaches for treatment of COVID-19.Journal of molecular medicine (Berlin, Germany) · 2020Review
- A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation.Journal of visualized experiments : JoVE · 2019Article
- Effects of Multiday Ethanol Intoxication on Postburn Inflammation, Lung Function, and Alveolar Macrophage Phenotype.Shock (Augusta, Ga.) · 2019Article
- Biofilm-induced profiles of immune response gene expression by oral epithelial cells.Molecular oral microbiology · 2019Article
- Roles of interleukin-11 during acute bacterial pneumonia.PloS one · 2019Article
- Integrative Physiology of Pneumonia.Physiological reviews · 2018Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
In bacterial pneumonia, lung damage resulting from epithelial cell injury is a major contributor to the severity of disease and, in some cases, can lead to long-term sequelae, especially in the setting of severe lung injury or acute respiratory distress syndrome. Leukemia inhibitory factor (LIF), a member of the IL-6 cytokine family, is a critical determinant of lung tissue protection during pneumonia, but the cellular sources of LIF and the signaling pathways leading to its production in the infected lung are not known. Here, we demonstrate that lung epithelium, specifically alveolar type II cells, is the predominant site of LIF transcript induction in pneumonic mouse lungs. Epithelial cell cultures were induced to express LIF by bacteria and by sterile bronchoalveolar lavage fluid from pneumonic mice. Reciprocal bone marrow chimera studies demonstrated that LIF deficiency in the nonhematopoietic compartment, but not LIF deficiency in hematopoietic cells, eliminated LIF induction during pneumonia. Although NF-κB RelA (p65) is essential for the expression of many cytokines during pneumonia, its targeted mutation in the lung epithelium was inconsequential for pneumonia-driven LIF induction. However, maximal expression of this epithelial-derived cytokine was dependent on NF-κB RelA in myeloid cells. Overall, our data suggest a signaling axis whereby activation of NF-κB RelA in myeloid cells promotes epithelial LIF induction during lung infections, representing a means through which these two cell types collaborate to improve tissue resilience during pneumonia.
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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.