ArticleThe American journal of pathology2012
Co-exposure to cigarette smoke and alcohol decreases airway epithelial cell cilia beating in a protein kinase Cε-dependent manner.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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Who cites it
35 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Pharmacological regulation of airway ciliary motility: endogenous mediators, pharmaceutical agents, and natural compounds with a focus on ginsenoside Rd.Journal of natural medicines · 2026Review
- Semaglutide and pioglitazone restore airway mucosal homeostasis by resolvingFrontiers in immunology · 2026Article
- Comparative effects of e-cigarette and conventional cigarette smoke on in vitro bronchial epithelial cell responses.Toxicology letters · 2025Article
- Zinc Protects against Swine Barn Dust-Induced Cilia Slowing.Biomolecules · 2024Article
- Synergistic Detrimental Effects of Cigarette Smoke, Alcohol, and SARS-CoV-2 in COPD Bronchial Epithelial Cells.Pathogens (Basel, Switzerland) · 2023Article
- Perspectives on precision cut lung slices-powerful tools for investigation of mechanisms and therapeutic targets in lung diseases.Frontiers in pharmacology · 2023Review
- Phosphorylation-dependent proteome of Marcks in ependyma during aging and behavioral homeostasis in the mouse forebrain.GeroScience · 2022Article
- Aldehyde Trapping by ADX-102 Is Protective against Cigarette Smoke and Alcohol Mediated Lung Cell Injury.Biomolecules · 2022Article
- Alcohol use disorder: A pre-existing condition for COVID-19?Alcohol (Fayetteville, N.Y.) · 2021Review
- Second hits exacerbate alcohol-related organ damage: an update.Alcohol and alcoholism (Oxford, Oxfordshire) · 2021Review
- Alcohol Use Disorders Are Associated With a Unique Impact on Airway Epithelial Cell Gene Expression.Alcoholism, clinical and experimental research · 2020Article
- Applications and Approaches for Three-Dimensional Precision-Cut Lung Slices. Disease Modeling and Drug Discovery.American journal of respiratory cell and molecular biology · 2020Review
- Preserving Airway Smooth Muscle Contraction in Precision-Cut Lung Slices.Scientific reports · 2020Article
- Dual Substance Use of Electronic Cigarettes and Alcohol.Frontiers in physiology · 2020Review
- The impact of alcohol use disorders on pulmonary immune cell inflammatory responses to Streptococcus pneumoniae.Alcohol (Fayetteville, N.Y.) · 2019Article
- Alcohol potentiates RSV-mediated injury to ciliated airway epithelium.Alcohol (Fayetteville, N.Y.) · 2019Article
- Redox regulation of motile cilia in airway disease.Redox biology · 2019Review
- Oxidative stress associated with aging activates protein kinase Cε, leading to cilia slowing.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Alcohol consumption impairs the ependymal cilia motility in the brain ventricles.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Alcohol use disorders are associated with increased lung infections and exacerbations of chronic lung diseases. Whereas the effects of cigarette smoke are well recognized, the interplay of smoke and alcohol in modulating lung diseases is not clear. Because innate lung defense is mechanically maintained by airway cilia action and protein kinase C (PKC)-activating agents slow ciliary beat frequency (CBF), we hypothesized that the combination of smoke and alcohol would decrease CBF in a PKC-dependent manner. Primary ciliated bronchial epithelial cells were exposed to 5% cigarette smoke extract plus100 mmol/L ethanol for up to 24 hours and assayed for CBF and PKCε. Smoke and alcohol co-exposure activated PKCε by 1 hour and decreased both CBF and total number of beating cilia by 6 hours. A specific activator of PKCε, DCP-LA, slowed CBF after maximal PKCε activation. Interestingly, activation of PKCε by smoke and alcohol was only observed in ciliated cells, not basal bronchial epithelium. In precision-cut mouse lung slices treated with smoke and alcohol, PKCε activation preceded CBF slowing. Correspondingly, increased PKCε activity and cilia slowing were only observed in mice co-exposed to smoke and alcohol, regardless of the sequence of the combination exposure. No decreases in CBF were observed in PKCε knockout mice co-exposed to smoke and alcohol. These data identify PKCε as a key regulator of cilia slowing in response to combined smoke and alcohol-induced lung injury.
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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.