ArticleJournal of immunology (Baltimore, Md. : 1950)2012
TLR signaling prevents hyperoxia-induced lung injury by protecting the alveolar epithelium from oxidant-mediated death.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. 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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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.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Inhibition of BRD4 activates the AKT-SIRT3 signaling pathway to suppress apoptosis and attenuate hyperoxia-induced lung injury.Frontiers in bioengineering and biotechnology · 2025Article
- Long-term survivors of murine sepsis are predisposed to enhanced LPS-induced lung injury and proinflammatory immune reprogramming.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Toll-like receptors, environmental caging, and lung dysbiosis.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Persistent Neuroinflammation and Brain-Specific Immune Priming in a Novel Survival Model of Murine Pneumosepsis.Shock (Augusta, Ga.) · 2020Article
- IRAK-M Regulates Monocyte Trafficking to the Lungs in Response to Bleomycin Challenge.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Macrophage HIF-1α mediates obesity-related adipose tissue dysfunction via interleukin-1 receptor-associated kinase M.American journal of physiology. Endocrinology and metabolism · 2020Article
- miR-21-5p Suppresses Mitophagy to Alleviate Hyperoxia-Induced Acute Lung Injury by Directly Targeting PGAM5.BioMed research international · 2020Article
- S100A8/A9 Drives Neuroinflammatory Priming and Protects against Anxiety-like Behavior after Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Bacterial Dissemination to the Brain in Sepsis.American journal of respiratory and critical care medicine · 2018Article
- Could Heme Oxygenase-1 Be a New Target for Therapeutic Intervention in Malaria-Associated Acute Lung Injury/Acute Respiratory Distress Syndrome?Frontiers in cellular and infection microbiology · 2018Review
- An endothelial TLR4-VEGFR2 pathway mediates lung protection against oxidant-induced injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Cecal Ligation and Puncture Results in Long-Term Central Nervous System Myeloid Inflammation.PloS one · 2016Article
- A Role for Low Density Lipoprotein Receptor-Related Protein 1 in the Cellular Uptake of Tissue Plasminogen Activator in the Lungs.Pharmaceutical research · 2016Article
- Epigenetic Regulation of Tolerance to Toll-Like Receptor Ligands in Alveolar Epithelial Cells.American journal of respiratory cell and molecular biology · 2015Article
- IRAK-M promotes alternative macrophage activation and fibroproliferation in bleomycin-induced lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Article
- Heme oxygenase in neonatal lung injury and repair.Antioxidants & redox signaling · 2014Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Mechanical ventilation using high oxygen tensions is often necessary to treat patients with respiratory failure. Recently, TLRs were identified as regulators of noninfectious oxidative lung injury. IRAK-M is an inhibitor of MyD88-dependent TLR signaling. Exposure of mice deficient in IRAK-M (IRAK-M(-/-)) to 95% oxygen resulted in reduced mortality compared with wild-type mice and occurred in association with decreased alveolar permeability and cell death. Using a bone marrow chimera model, we determined that IRAK-M's effects were mediated by structural cells rather than bone marrow-derived cells. We confirmed the expression of IRAK-M in alveolar epithelial cells (AECs) and showed that hyperoxia can induce the expression of this protein. In addition, IRAK-M(-/-) AECs exposed to hyperoxia experienced a decrease in cell death. IRAK-M may potentiate hyperoxic injury by suppression of key antioxidant pathways, because lungs and AECs isolated from IRAK-M(-/-) mice have increased expression/activity of heme oxygenase-1, a phase II antioxidant, and NF (erythroid-derived)-related factor-2, a transcription factor that initiates antioxidant generation. Treatment of IRAK-M(-/-) mice in vivo and IRAK-M(-/-) AECs in vitro with the heme oxygenase-1 inhibitor, tin protoporphyrin, substantially decreased survival and significantly reduced the number of live cells after hyperoxia exposure. Collectively, our data suggest that IRAK-M inhibits the induction of antioxidants essential for protecting the lungs against cell death, resulting in enhanced susceptibility to hyperoxic lung injury.
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