ArticleThe Journal of clinical investigation2020
Residual endotoxin induces primary graft dysfunction through ischemia/reperfusion-primed alveolar macrophages.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- How the Jacobson Award Catalyzed My Pursuit of Surgical Innovation.Journal of the American College of Surgeons · 2026Article
- Multi-omics analysis reveals the host-microbe interactions on the dysbiosis of tissue microbiota in male genital lichen sclerosus-induced urethral strictures.Microbiology spectrum · 2025Article
- Primary graft dysfunction after Lung transplantation: unveiling the role of innate immunity.Clinical and experimental immunology · 2025Article
- Inducible CCR2+ nonclassical monocytes mediate the regression of cancer metastasis.The Journal of clinical investigation · 2024Article
- Nanoparticle targeting of neutrophil glycolysis prevents lung ischemia-reperfusion injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- Cathepsin C from extracellular histone-induced M1 alveolar macrophages promotes NETosis during lung ischemia-reperfusion injury.Redox biology · 2024Article
- Lobar lung transplantation in the mouse.Journal of thoracic disease · 2024Article
- Smoking exposure-induced bronchus-associated lymphoid tissue in donor lungs does not prevent tolerance induction after transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- Multiple Shades of Gray-Macrophages in Acute Allograft Rejection.International journal of molecular sciences · 2023Review
- Alveolar Macrophages Participate in the Promotion of Influenza Virus Infection by Aflatoxin B1 at an Early Stage.Toxins · 2023Article
- SARS-CoV-2 N Protein Triggers Acute Lung Injury via Modulating Macrophage Activation and Infiltration in in vitro and in vivo.Journal of inflammation research · 2023Article
- IL-1β-dependent extravasation of preexisting lung-restricted autoantibodies during lung transplantation activates complement and mediates primary graft dysfunction.The Journal of clinical investigation · 2022Article
- miR-141 exacerbates lung ischemia-reperfusion injury by targeting EGFR/β-catenin axis-mediated autophagy.Aging · 2022Article
- ROS-activated CXCR2Experimental & molecular medicine · 2022Article
- CD14 blockade to prevent ischemic injury to donor organs.Transplant immunology · 2022Review
- Necroptosis triggers spatially restricted neutrophil-mediated vascular damage during lung ischemia reperfusion injury.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Microglial lnc-U90926 facilitates neutrophil infiltration in ischemic stroke via MDH2/CXCL2 axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Innate immunity in lung transplantation.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021Review
- Crosstalk between nonclassical monocytes and alveolar macrophages mediates transplant ischemia-reperfusion injury through classical monocyte recruitment.JCI insight · 2021Article
- Macrophages in Organ Transplantation.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
22 authors at 5 institutions in 1 country.
Funding
Abstract
Despite the widespread use of antibiotics, bacterial pneumonias in donors strongly predispose to the fatal syndrome of primary graft dysfunction (PGD) following lung transplantation. We report that bacterial endotoxin persists in human donor lungs after pathogen is cleared with antibiotics and is associated with neutrophil infiltration and PGD. In mouse models, depletion of tissue-resident alveolar macrophages (TRAMs) attenuated neutrophil recruitment in response to endotoxin as shown by compartmental staining and intravital imaging. Bone marrow chimeric mice revealed that neutrophils were recruited by TRAM through activation of TLR4 in a MyD88-dependent manner. Intriguingly, low levels of endotoxin, insufficient to cause donor lung injury, promoted TRAM-dependent production of CXCL2, increased neutrophil recruitment, and led to PGD, which was independent of donor NCMs. Reactive oxygen species (ROS) increased in human donor lungs starting from the warm-ischemia phase and were associated with increased transcription and translocation to the plasma membrane of TLR4 in donor TRAMs. Consistently, scavenging ROS or inhibiting their production to prevent TLR4 transcription/translocation or blockade of TLR4 or coreceptor CD14 on donor TRAMs prevented neutrophil recruitment in response to endotoxin and ameliorated PGD. Our studies demonstrate that residual endotoxin after successful treatment of donor bacterial pneumonia promotes PGD through ischemia/reperfusion-primed donor TRAMs.
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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.