ArticleLung2025
Alteration of the Secretome in Airway Epithelial Cells by Air Pollutants: Evidence from an Air-Liquid Interface Model.
Article in Lung, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Climate Change and Food Allergy: Adaptations and Risks at the Intersection of Environment and Health.Comprehensive reviews in food science and food safety · 2026Review
- Combined Exposure to Ragweed and House Dust Mite Exacerbates Airway Epithelial Barrier Dysfunction: A Multimodal Approach.Medicina (Kaunas, Lithuania) · 2026Article
- Unmasking the Impact of Air Pollution on Allergic Rhinitis.Clinical reviews in allergy & immunology · 2026Review
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.
Funding
Abstract
introductionWhile the structural damage to the airway epithelium from ozone (O₃) or diesel exhaust particles (DEP) is known, the common regulatory mechanisms activated during mixed exposures, which mirror real-world scenarios, remain poorly understood. This study aimed to identify shared molecular pathways initiated by exposure to O₃ and DEP using an in vitro air-liquid interface (ALI) model to understand the initial cellular responses.
methodsPolarized Calu-3 cell monolayers at the ALI were acutely exposed to non-cytotoxic O₃ or DEP. Barrier integrity was assessed via transepithelial electrical resistance (TEER) and FITC-dextran permeability. Gene expression of tight junctions and alarmin cytokines was quantified by qPCR, while the protein level of tight junctions was identified by immunofluorescence. The cellular secretome was comprehensively analyzed using label-free liquid chromatography-tandem mass spectrometry.
resultsBoth pollutants impaired barrier integrity, evidenced by decreased TEER and increased permeability, and induced a potent inflammatory response via upregulation of alarmin cytokines IL-25, IL-33, and TSLP. Critically, secretome analysis revealed that although O₃ and DEP initiated distinct upstream damage patterns, their responses converged on common downstream pathways, including the activation of Wnt signaling and antigen processing and presentation.
conclusionExposure to O₃ and DEP compromises airway epithelial barrier function and triggers a robust alarmin-driven inflammatory response. Our identification of convergent downstream pathways, such as Wnt signaling, provides crucial mechanistic insights into the shared pathophysiology of mixed pollutant exposure. These findings highlight potential therapeutic targets for mitigating the adverse health effects of complex air pollution.
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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.