ArticleThorax2016
Cigarette smokers have exaggerated alveolar barrier disruption in response to lipopolysaccharide inhalation.
Article in Thorax, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- Biochemical verification of tobacco use in ICU patients using point-of-care urinary cotinine.Critical care and resuscitation : journal of the Australasian Academy of Critical Care Medicine · 2026Article
- Short-term cigarette smoke exposure aggravates oxidative stress and airway inflammation induced by lipopolysaccharides.Frontiers in physiology · 2026Article
- Assessment of intestinal barrier integrity and associations with innate immune activation and metabolic syndrome in acutely ill, antipsychotic-free schizophrenia patients.Journal of neuroinflammation · 2025Article
- Chronic Exposure to Two Regimens of Waterpipe Smoke Elicits Lung Injury, Genotoxicity, and Mitochondrial Impairment with the Involvement of MAPKs Activation in Mice.International journal of molecular sciences · 2025Article
- Promoting immune defensive responses of epithelial cells in airway disease.Frontiers in allergy · 2025Review
- Environmental Risk Factors for Acute Respiratory Distress Syndrome.Clinics in chest medicine · 2024Review
- Endothelial knockdown of the tumor suppressor,American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Molecular Impact of Conventional and Electronic Cigarettes on Pulmonary Surfactant.International journal of molecular sciences · 2023Review
- Schisandrin A regulates the Nrf2 signaling pathway and inhibits NLRP3 inflammasome activation to interfere with pyroptosis in a mouse model of COPD.European journal of medical research · 2023Article
- Cigarette Smoke-Induced Respiratory Response: Insights into Cellular Processes and Biomarkers.Antioxidants (Basel, Switzerland) · 2023Review
- Strain-dependent lung transcriptomic differences in cigarette smoke and LPS models of lung injury in mice.Physiological genomics · 2023Article
- NLRP3 inflammasome activation in cigarette smoke priming for Pseudomonas aeruginosa-induced acute lung injury.Redox biology · 2022Article
- Aging-associated and CD4 T-cell-dependent ectopic CXCL13 activation predisposes to anti-PD-1 therapy-induced adverse events.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Compound K ameliorates airway inflammation and mucus secretion through the regulation of PKC signaling in vitro and in vivo.Journal of ginseng research · 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
- Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo.Antioxidants (Basel, Switzerland) · 2022Article
- Isorhamnetin Alleviates Airway Inflammation by Regulating the Nrf2/Keap1 Pathway in a Mouse Model of COPD.Frontiers in pharmacology · 2022Article
- A New Immortalized Human Alveolar Epithelial Cell Model to Study Lung Injury and Toxicity on a Breathing Lung-On-Chip System.Frontiers in toxicology · 2022Article
- Environmental Factors.Critical care clinics · 2021Review
- The Role of Interleukin-8 in Lung Inflammation and Injury: Implications for the Management of COVID-19 and Hyperinflammatory Acute Respiratory Distress Syndrome.Frontiers in pharmacology · 2021Review
Corrections and comments
- Commented on by
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
rationaleCigarette smoke exposure is associated with an increased risk of the acute respiratory distress syndrome (ARDS); however, the mechanisms underlying this relationship remain largely unknown.
objectiveTo assess pathways of lung injury and inflammation in smokers and non-smokers with and without lipopolysaccharide (LPS) inhalation using established biomarkers.
methodsWe measured plasma and bronchoalveolar lavage (BAL) biomarkers of inflammation and lung injury in smokers and non-smokers in two distinct cohorts of healthy volunteers, one unstimulated (n=20) and one undergoing 50 μg LPS inhalation (n=30). MEASUREMENTS AND MAIN
resultsAfter LPS inhalation, cigarette smokers had increased alveolar-capillary membrane permeability as measured by BAL total protein, compared with non-smokers (median 274 vs 208 μg/mL, p=0.04). Smokers had exaggerated inflammation compared with non-smokers, with increased BAL interleukin-1β (p=0.002), neutrophils (p=0.02), plasma interleukin-8 (p=0.003), and plasma matrix metalloproteinase-8 (p=0.006). Alveolar epithelial injury after LPS was more severe in smokers than non-smokers, with increased plasma (p=0.04) and decreased BAL (p=0.02) surfactant protein D. Finally, smokers had decreased BAL vascular endothelial growth factor (VEGF) (p<0.0001) with increased soluble VEGF receptor-1 (p=0.0001).
conclusionsCigarette smoke exposure may predispose to ARDS through an abnormal response to a 'second hit,' with increased alveolar-capillary membrane permeability, exaggerated inflammation, increased epithelial injury and endothelial dysfunction. LPS inhalation may serve as a useful experimental model for evaluation of the acute pulmonary effects of existing and new tobacco products.
Indexed as
Identifiers
What OpenQuestion holds
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.