ArticleAmerican journal of respiratory cell and molecular biology2015
Wood smoke enhances cigarette smoke-induced inflammation by inducing the aryl hydrocarbon receptor repressor in airway epithelial cells.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 43 citations in OpenAlex.
- Wood Smoke Exposure Alters Human Inflammatory Responses to Viral Infection in a Sex-Specific Manner. A Randomized, Placebo-controlled Study.American journal of respiratory and critical care medicine · 2019Trial
- Specialized pro-resolving mediators in vascular inflammation and atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Persistence of emphysema following cessation of cigarette smoke exposure requires a susceptibility factor.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Arachidonic Acid Metabolites in Self-collected Biospecimens Following Campfire Exposure: Exploring Non-invasive Biomarkers of Wildfire Health Effects.Environmental science & technology letters · 2024Article
- Chronic obstructive pulmonary disease related to wood smoke and impact of the combined exposure to tobacco.IJTLD open · 2024Article
- Imaging-based assessment of lung function in a population cooking indoors with biomass fuel: a pilot study.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- SNPs Sets in Codifying Genes for Xenobiotics-Processing Enzymes Are Associated with COPD Secondary to Biomass-Burning Smoke.Current issues in molecular biology · 2023Article
- Physicochemical and toxicological properties of wood smoke particulate matter as a function of wood species and combustion condition.Journal of hazardous materials · 2023Article
- Development of an Integrated Platform to Assess the Physicochemical and Toxicological Properties of Wood Combustion Particulate Matter.Chemical research in toxicology · 2022Article
- More than Meets the Eye: The Aryl Hydrocarbon Receptor is an Environmental Sensor, Physiological Regulator and a Therapeutic Target in Ocular Disease.Frontiers in toxicology · 2022Review
- The Impact of Air Pollution on the Course of Cystic Fibrosis: A Review.Frontiers in physiology · 2022Review
- Effects of Wood Smoke Constituents on Mucin Gene Expression in Mice and Human Airway Epithelial Cells and on Nasal Epithelia of Subjects with a Susceptibility Gene Variant inEnvironmental health perspectives · 2022Article
- Protective Role of Genetic Variants in HSP90 Genes-Complex in COPD Secondary to Biomass-Burning Smoke Exposure and Non-Severe COPD Forms in Tobacco Smoking Subjects.Current issues in molecular biology · 2021Article
- Cigarette smoke-induced alterations in blood: A review of research on DNA methylation and gene expression.Experimental and clinical psychopharmacology · 2021Review
- Transcriptomic Analysis of Right Ventricular Remodeling in Two Rat Models of Pulmonary Hypertension: Identification and Validation of Epithelial-to-Mesenchymal Transition in Human Right Ventricular Failure.Circulation. Heart failure · 2021Article
- An Examination of Risk Factors for Tobacco and Cannabis Smoke Exposure in Adolescents Using an Epigenetic Biomarker.Frontiers in psychiatry · 2021Article
- m6A RNA methylation regulators could contribute to the occurrence of chronic obstructive pulmonary disease.Journal of cellular and molecular medicine · 2020Article
- Meta-Analysis of Transcriptome Data Detected New Potential Players in Response to Dioxin Exposure in Humans.International journal of molecular sciences · 2020Article
- Quenching the fires: Pro-resolving mediators, air pollution, and smoking.Pharmacology & therapeutics · 2019Review
- The Aryl Hydrocarbon Receptor and the Maintenance of Lung Health.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Our previous studies showed that cigarette smokers who are exposed to wood smoke (WS) are at an increased risk for chronic bronchitis and reduced lung function. The present study was undertaken to determine the mechanisms for WS-induced adverse effects. We studied the effect of WS exposure using four cohorts of mice. C57Bl/6 mice were exposed for 4 or 12 weeks to filtered air, to 10 mg/m(3) WS for 2 h/d, to 250 mg/m(3) cigarette smoke (CS) for 6 h/d, or to CS followed by WS (CW). Inflammation was absent in the filtered air and WS groups, but enhanced by twofold in the bronchoalveolar lavage of the CW compared with CS group as measured by neutrophil numbers and levels of the neutrophil chemoattractant, keratinocyte-derived chemokine. The levels of the anti-inflammatory lipoxin, lipoxin A4, were reduced by threefold along with cyclo-oxygenase (COX)-2 and microsomal prostaglandin E synthase (mPGES)-1 in airway epithelial cells and PGE2 levels in the bronchoalveolar lavage of CW compared with CS mice. We replicated, in primary human airway epithelial cells, the changes observed in mice. Immunoprecipitations showed that WS blocked the interaction of aryl hydrocarbon receptor (AHR) with AHR nuclear transporter to reduce expression of COX-2 and mPGES-1 by increasing expression of AHR repressor (AHRR). Collectively, these studies show that exposure to low concentrations of WS enhanced CS-induced inflammation by inducing AHRR expression to suppress AHR, COX-2, and mPGES-1 expression, and levels of PGE2 and lipoxin A4. Therefore, AHRR is a potential therapeutic target for WS-associated exacerbations of CS-induced inflammation.
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.