ArticleAmerican journal of respiratory and critical care medicine2014
Hyaluronan contributes to bronchiolitis obliterans syndrome and stimulates lung allograft rejection through activation of innate immunity.
Article in American journal of respiratory and critical care medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 94 citations in OpenAlex.
- Multi-omics biomarkers of endothelial dysregulation preceding chronic lung allograft dysfunction: A prospective cohort study.PLoS medicine · 2026Article
- Lymphatic disruption drives lung transplant fibrosis through interleukin-1-mediated hyaluronan accumulation.Science translational medicine · 2026Article
- Identification and validation of a threshold for early posttransplant bronchoalveolar fluid hyaluronan that distinguishes lung recipients at risk for chronic lung allograft 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
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- Mitsugumin 53 mitigation of ischemia-reperfusion injury in a mouse model.The Journal of thoracic and cardiovascular surgery · 2024Article
- Lymphatic vessel: origin, heterogeneity, biological functions, and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Deciphering the Complexity of the Immune Cell Landscape in Kidney Allograft Rejection.Transplant international : official journal of the European Society for Organ Transplantation · 2024Review
- JAK-STAT activation contributes to cytotoxic T cell-mediated basal cell death in human chronic lung allograft dysfunction.JCI insight · 2023Article
- The lymphatic vasculature in lung function and respiratory disease.Frontiers in medicine · 2023Review
- Reprogramming alveolar macrophage responses to TGF-β reveals CCR2+ monocyte activity that promotes bronchiolitis obliterans syndrome.The Journal of clinical investigation · 2022Article
- Modulation of hyaluronan signaling as a therapeutic target in human disease.Pharmacology & therapeutics · 2022Review
- Novel approaches for long-term lung transplant survival.Frontiers in immunology · 2022Review
- Blocking hyaluronan synthesis alleviates acute lung allograft rejection.JCI insight · 2021Article
- Innate immunity in lung transplantation.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021Review
- Intragraft Hyaluronan Increases in Association With Acute Lung Transplant Rejection.Transplantation direct · 2021Article
- Sterile inflammation in thoracic transplantation.Cellular and molecular life sciences : CMLS · 2021Review
- Connective Tissue Growth Factor Is Overexpressed in Explant Lung Tissue and Broncho-Alveolar Lavage in Transplant-Related Pulmonary Fibrosis.Frontiers in immunology · 2021Article
- Untangling Local Pro-Inflammatory, Reparative, and Regulatory Damage-Associated Molecular-Patterns (DAMPs) Pathways to Improve Transplant Outcomes.Frontiers in immunology · 2021Review
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleAlthough innate immunity is increasingly recognized to contribute to lung allograft rejection, the significance of endogenous innate ligands, such as hyaluronan (HA) fragments, in clinical or experimental lung transplantation is uncertain.
objectivesTo determine if HA is associated with clinical bronchiolitis obliterans syndrome (BOS) in lung transplant recipients, and evaluate the effect of low- or high-molecular-weight HA on experimental lung allograft rejection, including dependence on innate signaling pathways or effector cells.
methodsHA concentrations were measured in bronchoalveolar lavage and plasma samples from lung recipients with or without established BOS. BOS and normal lung tissues were assessed for HA localization and expression of HA synthases. Murine orthotopic lung recipients with established tolerance were treated with low- or high-molecular-weight HA under varied experimental conditions, including Toll-like receptor (TLR) 2/4 and myeloid differentiation protein 88 deficiency and neutrophil depletion. MEASUREMENTS AND MAIN
resultsHA localized within areas of intraluminal small airways fibrosis in BOS lung tissue. Moreover, transcripts for HA synthase enzymes were significantly elevated in BOS versus normal lung tissues and both lavage fluid and plasma HA concentrations were increased in recipients with BOS. Treatment with low-molecular-weight HA abrogated tolerance in murine orthotopic lung recipients in a TLR2/4- and myeloid differentiation protein 88-dependent fashion and drove expansion of alloantigen-specific T lymphocytes. Additionally, TLR-dependent signals stimulated neutrophilia that promoted rejection. In contrast, high-molecular-weight HA attenuated basal allograft inflammation.
conclusionsThese data suggest that accumulation of HA could contribute to BOS by directly activating innate immune signaling pathways that promote allograft rejection and neutrophilia.
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