ArticleScience translational medicine2017
Donor pulmonary intravascular nonclassical monocytes recruit recipient neutrophils and mediate primary lung allograft dysfunction.
Article in Science translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05950724 (RENAL), which is not on this map. Cited by 66 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
RENAL: Randomized Clinical Trial of TNF-alpha Inhibitor for Improving Renal Dysfunction and Primary Graft Dysfunction After Lung Transplant
Who cites it
66 citing papers in PubMed, 86 citations in OpenAlex.
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- GSK'872 mitigates ischemia-reperfusion injury in rat lung transplants by regulating PANoptosis and inflammation in cell type specific manner.Cell communication and signaling : CCS · 2026Article
- Trem1 regulates neutrophil metabolism and recruitment in lung ischemia-reperfusion injury.Redox biology · 2026Article
- How the Jacobson Award Catalyzed My Pursuit of Surgical Innovation.Journal of the American College of Surgeons · 2026Article
- Toward development of a dynamic supramolecular peptide therapy for acute ischemic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Article
- Neutrophil-based delivery platforms: from natural mechanisms to engineered therapeutics.Theranostics · 2026Review
- Primary Graft Dysfunction in Lung Transplantation: An Overview of the Molecular Mechanisms.International journal of molecular sciences · 2025Review
- Targeting mitochondrial complex I of CD177Cell reports. Medicine · 2025Article
- Acute kidney injury triggers hypoxemia by lung intravascular neutrophil retention that reduces capillary blood flow.The Journal of clinical investigation · 2025Article
- EdU tracking of leukocyte recruitment in mouse models of ischemic stroke and sterile lung inflammation.Journal of cell science · 2025Article
- Lung allograft dysbiosis associates with immune response and primary graft dysfunction.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025Article
- Chronic Lung Allograft Dysfunction: Clinical Manifestations and Immunologic Mechanisms.Transplantation · 2025Review
- Article
- Primary graft dysfunction after Lung transplantation: unveiling the role of innate immunity.Clinical and experimental immunology · 2025Article
- Predictive value of the monocyte count for determining the risk of postoperative moderate-to-severe ARDS in patients undergoing one-lung ventilation during radical treatment of esophageal cancer.Frontiers in medicine · 2025Article
- Improving lung allograft function in the early post-operative period through the inhibition of pyroptosis.Medical review (2021) · 2024Review
- Inducible CCR2+ nonclassical monocytes mediate the regression of cancer metastasis.The Journal of clinical investigation · 2024Article
- Cathepsin C from extracellular histone-induced M1 alveolar macrophages promotes NETosis during lung ischemia-reperfusion injury.Redox biology · 2024Article
- Temporal correlation between postreperfusion complement deposition and severe primary graft dysfunction in lung allografts.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
Primary graft dysfunction is the predominant driver of mortality and graft loss after lung transplantation. Recruitment of neutrophils as a result of ischemia-reperfusion injury is thought to cause primary graft dysfunction; however, the mechanisms that regulate neutrophil influx into the injured lung are incompletely understood. We found that donor-derived intravascular nonclassical monocytes (NCMs) are retained in human and murine donor lungs used in transplantation and can be visualized at sites of endothelial injury after reperfusion. When NCMs in the donor lungs were depleted, either pharmacologically or genetically, neutrophil influx and lung graft injury were attenuated in both allogeneic and syngeneic models. Similar protection was observed when the patrolling function of donor NCMs was impaired by deletion of the fractalkine receptor CX3CR1. Unbiased transcriptomic profiling revealed up-regulation of MyD88 pathway genes and a key neutrophil chemoattractant, CXCL2, in donor-derived NCMs after reperfusion. Reconstitution of NCM-depleted donor lungs with wild-type but not MyD88-deficient NCMs rescued neutrophil migration. Donor NCMs, through MyD88 signaling, were responsible for CXCL2 production in the allograft and neutralization of CXCL2 attenuated neutrophil influx. These findings suggest that therapies to deplete or inhibit NCMs in donor lung might ameliorate primary graft dysfunction with minimal toxicity to the recipient.
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Registered trials
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.