ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Double-hit mouse model of cigarette smoke priming for acute lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Short-term cigarette smoke exposure aggravates oxidative stress and airway inflammation induced by lipopolysaccharides.Frontiers in physiology · 2026Article
- Integrative single-cell RNA and ATAC sequencing reveals the impact of chronic cigarette smoking on lung epithelial responses to influenza and hyperoxia.Respiratory research · 2025Article
- Experimental animal models of acute respiratory distress syndrome: one-hit and two-hit establishment application.Frontiers in immunology · 2025Review
- The Potential Role of Cigarette Smoke, Elastic Fibers, and Secondary Lung Injury in the Transition of Pulmonary Emphysema to Combined Pulmonary Fibrosis and Emphysema.International journal of molecular sciences · 2024Article
- Endothelial knockdown of the tumor suppressor,American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Type V collagen-induced nasal tolerance prevents lung damage in an experimental model: new evidence of autoimmunity to collagen V in COPD.Frontiers in immunology · 2024Article
- IL-1β-mediated adaptive reprogramming of endogenous human cardiac fibroblasts to cells with immune features during fibrotic remodeling.Communications biology · 2023Article
- Strain-dependent lung transcriptomic differences in cigarette smoke and LPS models of lung injury in mice.Physiological genomics · 2023Article
- Silencing circPalm2 inhibits sepsis-induced acute lung injury by sponging miR-376b-3p and targeting MAP3K1.Toxicological research · 2023Article
- Synergistic Effects of Resistive Breathing on Endotoxin-Induced Lung Injury in Mice.International journal of chronic obstructive pulmonary disease · 2023Article
- NLRP3 inflammasome activation in cigarette smoke priming for Pseudomonas aeruginosa-induced acute lung injury.Redox biology · 2022Article
- Cigarette Smoke Exposure and Acute Respiratory Distress Syndrome in Sepsis: Epidemiology, Clinical Features, and Biologic Markers.American journal of respiratory and critical care medicine · 2022Article
- Cyclooxygenase-2 deficiency attenuates lipopolysaccharide-induced inflammation, apoptosis, and acute lung injury in adult mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- CIGARETTE SMOKING INCREASES THE RISK OF ACUTE RESPIRATORY DISTRESS SYNDROME.Transactions of the American Clinical and Climatological Association · 2022Article
- Loss of Endothelial WWOX: A Risk Factor for ARDS in Smokers?American journal of respiratory cell and molecular biology · 2021Article
- Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.American journal of respiratory cell and molecular biology · 2020Article
- Article
- CircC3P1 attenuated pro-inflammatory cytokine production and cell apoptosis in acute lung injury induced by sepsis through modulating miR-21.Journal of cellular and molecular medicine · 2020Article
- Cigarette Smoke Triggers IL-33-associated Inflammation in a Model of Late-Stage Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2019Article
- Immunological Regulation of Vascular Inflammation During Cancer Metastasis.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiological studies indicate that cigarette smoking (CS) increases the risk and severity of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). The mechanism is not understood, at least in part because of lack of animal models that reproduce the key features of the CS priming process. In this study, using two strains of mice, we characterized a double-hit mouse model of ALI induced by CS priming of injury caused by lipopolysaccharide (LPS). C57BL/6 and AKR mice were preexposed to CS briefly (3 h) or subacutely (3 wk) before intratracheal instillation of LPS and ALI was assessed 18 h after LPS administration by measuring lung static compliance, lung edema, vascular permeability, inflammation, and alveolar apoptosis. We found that as little as 3 h of exposure to CS enhanced LPS-induced ALI in both strains of mice. Similar exacerbating effects were observed after 3 wk of preexposure to CS. However, there was a strain difference in susceptibility to CS priming for ALI, with a greater effect in AKR mice. The key features we observed suggest that 3 wk of CS preexposure of AKR mice is a reproducible, clinically relevant animal model that is useful for studying mechanisms and treatment of CS priming for a second-hit-induced ALI. Our data also support the concept that increased susceptibility to ALI/ARDS is an important adverse health consequence of CS exposure that needs to be taken into consideration when treating critically ill individuals.
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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.