ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019
Mechanism of pulmonary immunosuppression: extrapulmonary burn injury suppresses bacterial endotoxin-induced pulmonary neutrophil recruitment and neutrophil extracellular trap (NET) formation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Neutrophil extracellular traps in ischemic stroke: mechanisms, clinical implications, and therapeutic potential.Frontiers in neurology · 2025Review
- Elevation of neutrophil-derived factors in patients after multiple trauma.Journal of cellular and molecular medicine · 2023Article
- Effect of blended protein nutritional support on reducing burn-induced inflammation and organ injury.Nutrition research and practice · 2022Article
- Microfluidic capture of chromatin fibres measures neutrophil extracellular traps (NETs) released in a drop of human blood.Lab on a chip · 2022Article
- Severity of thermal burn injury is associated with systemic neutrophil activation.Scientific reports · 2022Article
- Lipocalin-2 in neutrophils induces ferroptosis in septic cardiac dysfunctionFrontiers in cardiovascular medicine · 2022Article
- Machine learning links different gene patterns of viral infection to immunosuppression and immune-related biomarkers in severe burns.Frontiers in immunology · 2022Article
- Recent Advances in Experimental Burn Models.Biology · 2021Review
- NETosis in the pathogenesis of acute lung injury following cutaneous chemical burns.JCI insight · 2021Article
- Neutrophil extracellular traps are not produced in pediatric patients with one-lung ventilation: a prospective, single-center, observational study.Translational pediatrics · 2020Article
- The Metabolic Basis of Immune Dysfunction Following Sepsis and Trauma.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Pulmonary immunosuppression often occurs after burn injury (BI). However, the reasons for BI-induced pulmonary immunosuppression are not clearly understood. Neutrophil recruitment and neutrophil extracellular trap (NET) formation (NETosis) are important components of a robust pulmonary immune response, and we hypothesized that pulmonary inflammation and NETosis are defective after BI. To test this hypothesis, we established a mouse model with intranasal LPS instillation in the presence or absence of BI (15% of body surface burn) and determined the degree of immune cell infiltration, NETosis, and the cytokine levels in the airways and blood on d 2. Presence of LPS recruited monocytes and large numbers of neutrophils to the airways and induced NETosis (citrullinated histone H3, DNA, myeloperoxidase). By contrast, BI significantly reduced LPS-mediated leukocyte recruitment and NETosis. This BI-induced immunosuppression is attributable to the reduction of chemokine (C-C motif) ligand (CCL) 2 (monocyte chemoattractant protein 1) and CCL3 (macrophage inflammatory protein 1α). BI also suppressed LPS-induced increase in IL-17A, IL-17C, and IL-17E/IL-25 levels in the airways. Therefore, BI-mediated reduction in leukocyte recruitment and NETosis in the lungs are attributable to these cytokines. Regulating the levels of some of these key cytokines represents a potential therapeutic option for mitigating BI-mediated pulmonary immunosuppression.-Sakuma, M., Khan, M. A. S., Yasuhara, S., Martyn, J. A., Palaniyar, N. Mechanism of pulmonary immunosuppression: extrapulmonary burn injury suppresses bacterial endotoxin-induced pulmonary neutrophil recruitment and neutrophil extracellular trap (NET) formation.
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Registered trials
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