ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
NADPH oxidase mediates synergistic effects of IL-17 and TNF-α on CXCL1 expression by epithelial cells after lung ischemia-reperfusion.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- Extracellular Superoxide Dismutase in Acute Respiratory Distress Syndrome: Pathogenic Mechanisms and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Institut Georges Lopez-2M as a Novel Lung Preservation Solution Attenuates Ischemia-Reperfusion Injury in a RatTransplant international : official journal of the European Society for Organ Transplantation · 2026Article
- γδCellular & molecular immunology · 2025Article
- Lipoxin AFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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
- Epithelial Na+ Channels, Immune Cells, and Salt.Annual review of physiology · 2025Review
- Primary graft dysfunction after Lung transplantation: unveiling the role of innate immunity.Clinical and experimental immunology · 2025Article
- Restoration of Type 17 immune signaling is not sufficient for protection during influenza-associated pulmonary aspergillosis.Frontiers in immunology · 2025Article
- Restoration of Type 17 immune signaling is not sufficient for protection during influenza-associated pulmonary aspergillosis.bioRxiv : the preprint server for biology · 2024Article
- Advances in lung ischemia/reperfusion injury: unraveling the role of innate immunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Transcriptome analysis revealed that ischemic post-conditioning suppressed the expression of inflammatory genes in lung ischemia-reperfusion injury.Frontiers in genetics · 2024Article
- Hemopexin alleviates sterile inflammation in ischemia-reperfusion-induced lung injury.Frontiers in immunology · 2024Article
- Resolution of post-lung transplant ischemia-reperfusion injury is modulated via Resolvin D1-FPR2 and Maresin 1-LGR6 signaling.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2023Article
- Application of dexmedetomidine for lung injury in elderly patients undergoing one-lung ventilation.Archives of medical science : AMS · 2023Article
- Phagocytosis is a primary determinant of pulmonary clearance of clinicalFrontiers in cellular and infection microbiology · 2023Article
- The Potential Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Cardiovascular System, Respiratory System and Skin.International journal of molecular sciences · 2022Review
- Alveolar type 2 epithelial cell senescence and radiation-induced pulmonary fibrosis.Frontiers in cell and developmental biology · 2022Review
- Role of inflammation, immunity, and oxidative stress in hypertension: New insights and potential therapeutic targets.Frontiers in immunology · 2022Review
- Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques.Journal of inflammation research · 2022Review
- The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review.Frontiers in medicine · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ischemia-reperfusion (I/R) injury leads to increased mortality and morbidity in lung transplant patients. Lung I/R injury involves inflammation contributed by innate immune responses. IL-17 and TNF-α, from iNKT cells and alveolar macrophages, respectively, contribute importantly to lung I/R injury. This study tests the hypothesis that IL-17 and TNF-α synergistically mediate CXCL1 (a potent neutrophil chemokine) production by alveolar type II epithelial (ATII) cells via an NADPH oxidase-dependent mechanism during lung I/R. Using a hilar clamp model, wild-type and p47(phox-/-) (NADPH oxidase-deficient) mice underwent left lung I/R, with or without recombinant IL-17 and/or TNF-α treatment. Wild-type mice undergoing I/R treated with combined IL-17 and TNF-α had significantly enhanced lung dysfunction, edema, CXCL1 production, and neutrophil infiltration compared with treatment with IL-17 or TNF-α alone. However, p47(phox-/-) mice had significantly less pulmonary dysfunction, CXCL1 production, and lung injury after I/R that was not enhanced by combined IL-17-TNF-α treatment. Moreover, in an acute in vitro hypoxia-reoxygenation model, murine ATII cells showed a multifold synergistic increase in CXCL1 expression after combined IL-17-TNF-α treatment compared with treatment with either cytokine alone, which was significantly attenuated by an NADPH oxidase inhibitor. Conditioned media transfer from hypoxia-reoxygenation-exposed iNKT cells and macrophages, major sources of IL-17 and TNF-α, respectively, to ATII cells significantly enhanced CXCL1 production, which was blocked by NADPH oxidase inhibitor. These results demonstrate that IL-17 and TNF-α synergistically mediate CXCL1 production by ATII cells after I/R, via an NADPH oxidase-dependent mechanism, to induce neutrophil infiltration and lung I/R injury.
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