ArticleJCI insight2021
Crosstalk between nonclassical monocytes and alveolar macrophages mediates transplant ischemia-reperfusion injury through classical monocyte recruitment.
Article in JCI insight, 2021. 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 37 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
37 citing papers in PubMed, 60 citations in OpenAlex.
- 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
- B6 Donor Lungs Develop Chronic Lung Allograft Dysfunction-like Pathology Across Histocompatibility Mismatches in Murine Lung Transplantation.Transplantation direct · 2026Article
- Alveolus-on-a-chip: A Novel Tool for Modeling Lung Transplant Cold Storage Ischemia/Reperfusion Injury.Transplantation · 2026Article
- Article
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- The role of macrophage polarization in organ transplantation: research progress on impact on graft injury, repair, and fibrosis.Frontiers in immunology · 2026Review
- The Myeloid-T Lymphocyte Axis in Chronic Lung Allograft Rejection: Emerging Insights into the Immune Circuitry Driving Fibrosis.Results and problems in cell differentiation · 2026Review
- B lymphocytes contribute Angiotensin II induced cardiac hypertrophy.Scientific reports · 2025Article
- 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
- MiR-146a engineered extracellular vesicles derived from mesenchymal stromal cells more potently attenuate ischaemia-reperfusion injury in lung transplantation.Clinical and translational medicine · 2025Article
- Chronic Lung Allograft Dysfunction: Clinical Manifestations and Immunologic Mechanisms.Transplantation · 2025Review
- Monocytes and interstitial macrophages contribute to hypoxic pulmonary hypertension.The Journal of clinical investigation · 2025Article
- Primary graft dysfunction after Lung transplantation: unveiling the role of innate immunity.Clinical and experimental immunology · 2025Article
- Preconditioning donors with corticosteroids improves early lung graft immunity.Frontiers in immunology · 2025Article
- Choroid plexus CCL2‒CCR2 signaling orchestrates macrophage recruitment and cerebrospinal fluid hypersecretion in hydrocephalus.Acta pharmaceutica Sinica. B · 2024Article
- Inducible CCR2+ nonclassical monocytes mediate the regression of cancer metastasis.The Journal of clinical investigation · 2024Article
- Improving lung allograft function in the early post-operative period through the inhibition of pyroptosis.Medical review (2021) · 2024Review
- 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
Corrections and comments
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Authors and funding
21 authors at 4 institutions in 1 country.
Funding
Abstract
Primary graft dysfunction (PGD) is the predominant cause of early graft loss following lung transplantation. We recently demonstrated that donor pulmonary intravascular nonclassical monocytes (NCM) initiate neutrophil recruitment. Simultaneously, host-origin classical monocytes (CM) permeabilize the vascular endothelium to allow neutrophil extravasation necessary for PGD. Here, we show that a CCL2-CCR2 axis is necessary for CM recruitment. Surprisingly, although intravital imaging and multichannel flow cytometry revealed that depletion of donor NCM abrogated CM recruitment, single cell RNA sequencing identified donor alveolar macrophages (AM) as predominant CCL2 secretors. Unbiased transcriptomic analysis of murine tissues combined with murine KOs and chimeras indicated that IL-1β production by donor NCM was responsible for the early activation of AM and CCL2 release. IL-1β production by NCM was NLRP3 inflammasome dependent and inhibited by treatment with a clinically approved sulphonylurea. Production of CCL2 in the donor AM occurred through IL-1R-dependent activation of the PKC and NF-κB pathway. Accordingly, we show that IL-1β-dependent paracrine interaction between donor NCM and AM leads to recruitment of recipient CM necessary for PGD. Since depletion of donor NCM, IL-1β, or IL-1R antagonism and inflammasome inhibition abrogated recruitment of CM and PGD and are feasible using FDA-approved compounds, our findings may have potential for clinical translation.
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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.