ArticleScientific reports2019
Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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
23 citing papers in PubMed, 51 citations in OpenAlex.
- DifferentialACS ES&T air · 2025Article
- Wildfire and asthma - The prospective interventions.The World Allergy Organization journal · 2025Review
- Environmental Risk Factors for Acute Respiratory Distress Syndrome.Clinics in chest medicine · 2024Review
- Autoimmune Diseases Following Environmental Disasters: A Narrative Review of the Literature.Healthcare (Basel, Switzerland) · 2024Review
- Assessment of wood smoke induced pulmonary toxicity in normal- and chronic bronchitis-like bronchial and alveolar lung mucosa models at air-liquid interface.Respiratory research · 2024Article
- Decreased fucosylation impacts epithelial integrity and increases risk for COPD.bioRxiv : the preprint server for biology · 2023Article
- Global warming and implications for epithelial barrier disruption and respiratory and dermatologic allergic diseases.The Journal of allergy and clinical immunology · 2023Review
- Elevated PLAUR is observed in the airway epithelium of asthma patients and blocking improves barrier integrity.Clinical and translational allergy · 2023Article
- Lung cancer associated with combustion particles and fine particulate matter (PMBiochemical pharmacology · 2023Review
- The Effects of Wildfire Smoke on Asthma and Allergy.Current allergy and asthma reports · 2023Review
- Deletion of sphingosine kinase 2 attenuates cigarette smoke-mediated chronic obstructive pulmonary disease-like symptoms by reducing lung inflammation.Biomolecules & biomedicine · 2023Article
- Exposure to local, source-specific ambient air pollution during pregnancy and autism in children: a cohort study from southern Sweden.Scientific reports · 2023Article
- Liquid application dosing alters the physiology of air-liquid interface (ALI) primary human bronchial epithelial cell/lung fibroblast co-cultures andFrontiers in toxicology · 2023Article
- Review
- Article
- COPD in Firefighters: A Specific Event-Related Condition Rather than a Common Occupational Respiratory Disorder.Medicina (Kaunas, Lithuania) · 2022Review
- Article
- The Impact of Environmental Pollutants on Barrier Dysfunction in Respiratory Disease.Allergy, asthma & immunology research · 2021Review
- Environmental Factors.Critical care clinics · 2021Review
- Effects of Air Pollutants on Airway Diseases.International journal of environmental research and public health · 2021Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Wildfire smoke induces acute pulmonary distress and is of particular concern to risk groups such as the sick and elderly. Wood smoke (WS) contains many of the same toxic compounds as those found in cigarette smoke (CS) including polycyclic aromatic hydrocarbons, carbon monoxide, and free radicals. CS is a well-established risk factor for respiratory diseases such as asthma and COPD. Limited studies investigating the biological effects of WS on the airway epithelium have been performed. Using a cell culture-based model, we assessed the effects of a WS-infused solution on alveolar epithelial barrier function, cell migration, and survival. The average geometric mean of particles in the WS was 178 nm. GC/MS analysis of the WS solution identified phenolic and cellulosic compounds. WS exposure resulted in a significant reduction in barrier function, which peaked after 24 hours of continuous exposure. The junctional protein E-cadherin showed a prominent reduction in response to increasing concentrations of WS. Furthermore, WS significantly repressed cell migration following injury to the cell monolayer. There was no difference in cell viability following WS exposure. Mechanistically, WS exposure induced activation of the p44/42, but not p38, MAPK signaling pathway, and inhibition of p44/42 phosphorylation prevented the disruption of barrier function and loss of E-cadherin staining. Thus, WS may contribute to the breakdown of alveolar structure and function through a p44/42 MAPK-dependent pathway and may lead to the development and/or exacerbation of respiratory pathologies with chronic exposure.
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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.