ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
Blocking CXCL1-dependent neutrophil recruitment prevents immune damage and reduces pulmonary bacterial infection after inhalation injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- Neutrophil immunometabolism in ACLF and sepsis: mechanisms, dysfunction, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Glycolysis-Related Genes,Cardiology research · 2025Article
- Temporal changes in the protein cargo of extracellular vesicles and resultant immune reprogramming after severe burn injury in humans and mice.Frontiers in immunology · 2025Article
- MULTIMODAL NUCLEAR FACTOR-ERYTHROID-2-RELATED FACTOR (NRF2) THERAPY IN THE CONTEXT OF MAMMALIAN TARGET OF RAPAMYCIN (MTOR) INHIBITION REPROGRAMS THE ACUTE SYSTEMIC AND PULMONARY IMMUNE RESPONSE AFTER COMBINED BURN AND INHALATION INJURY.Shock (Augusta, Ga.) · 2024Article
- "Air That Once Was Breath" Part 1: Wildfire-Smoke-Induced Mechanisms of Airway Inflammation - "Climate Change, Allergy and Immunology" Special IAAI Article Collection: Collegium Internationale Allergologicum Update 2023.International archives of allergy and immunology · 2024Review
- Characterization of the Basal and mTOR-Dependent Acute Pulmonary and Systemic Immune Response in a Murine Model of Combined Burn and Inhalation Injury.International journal of molecular sciences · 2022Article
- Early non-neutralizing, afucosylated antibody responses are associated with COVID-19 severity.Science translational medicine · 2022Article
- Severity of thermal burn injury is associated with systemic neutrophil activation.Scientific reports · 2022Article
- The EGFR/ErbB inhibitor neratinib modifies the neutrophil phosphoproteome and promotes apoptosis and clearance by airway macrophages.Frontiers in immunology · 2022Article
- Plasma extracellular vesicles released after severe burn injury modulate macrophage phenotype and function.Journal of leukocyte biology · 2022Article
- Burn Injury Induces Proinflammatory Plasma Extracellular Vesicles That Associate with Length of Hospital Stay in Women: CRP and SAA1 as Potential Prognostic Indicators.International journal of molecular sciences · 2021Article
- Development of novel nanofibers targeted to smoke-injured lungs.Biomaterials · 2021Article
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
- Radiotherapy programs neutrophils to an antitumor phenotype by inducing mesenchymal-epithelial transition.Translational lung cancer research · 2021Article
- Early local neutralization of CC16 in sepsis‑induced ALI following blunt chest trauma leads to delayed mortality without benefitting overall survival.International journal of molecular medicine · 2020Article
- A comparative study of a preclinical survival model of smoke inhalation injury in mice and rats.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Emerging therapies for smoke inhalation injury: a review.Journal of translational medicine · 2020Review
- Increased Lung Catalase Activity Confers Protection Against Experimental RSV Infection.Scientific reports · 2020Article
- G-CSFR antagonism reduces neutrophilic inflammation during pneumococcal and influenza respiratory infections without compromising clearance.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Smoke inhalation associated with structural fires, wildfires, or explosions leads to lung injury, for which innovative and clinically relevant animal models are needed to develop effective therapeutics. We have previously reported that damage-associated molecular patterns (DAMPs) and anti-inflammatory cytokines correlate with infectious complications in patients diagnosed with inhalational injury. In this study, we describe a novel and translational murine model of acute inhalational injury characterized by an accumulation of protein and neutrophils in the bronchoalveolar space, as well as histological evidence of tissue damage. Mice were anesthetized, and a cannula was placed in the trachea and exposed to smoldering plywood smoke three times for 2-min intervals in a smoke chamber. Here we demonstrate that this model recapitulates clinically relevant phenotypes, including early release of double-stranded DNA (dsDNA), IL-10, monocyte chemoattractant protein (MCP)-1, and CXCL1 along with neutrophilia early after injury, accompanied by subsequent susceptibility to opportunistic infection with Pseudomonas aeruginosa. Further investigation of the model, and in turn a reanalysis of patient samples, revealed a late release of the DAMP hyaluronic acid (HA) from the lung. Using nitric oxide synthase-deficient mice, we found that Nos2 was required for increases in IL-10, MCP-1, and HA following injury but not release of dsDNA, CXCL1 expression, early neutrophilia, or susceptibility to opportunistic infection. Depletion of CXCL1 attenuated early neutrophil recruitment, leading to decreased histopathology scores and improved bacterial clearance in this model of smoke inhalation. Together, these data highlight the potential therapeutic benefit of attenuating neutrophil recruitment in the first 24 h after injury in patients.
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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.