ArticleScientific reports2022
Modulation of mouse laryngeal inflammatory and immune cell responses by low and high doses of mainstream cigarette smoke.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Laryngeal Basal Cell Response to Cigarette Smoke and E-Cigarette Aerosol Exposures.The Laryngoscope · 2026Article
- Review
- Gut-larynx axis and its contribution to laryngeal immunity.mSystems · 2025Article
- Genetic diversity leads to differential inflammatory responses to cigarette smoke in mice.Physiological reports · 2025Article
- Effects of Short-term Electronic(e)-Cigarette Aerosol Exposure in the Mouse Larynx.The Laryngoscope · 2024Article
- Method for Collecting Single Epithelial Cells from the Mouse Larynx.The Laryngoscope · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cigarette smoking is a major risk factor for laryngeal diseases. Despite well-documented cigarette smoke (CS) induced laryngeal histopathological changes, the underlying immunopathological mechanisms remain largely unexplored. The goal of this study was to evaluate inflammatory and immune cell responses in a CS-exposed larynx. Specifically, we used a 4-week subacute whole-body CS inhalation mouse model to assess these responses in the laryngeal mucosa upon exposure to low (LD; 1 h/day) and high dose (HD; 4 h/day) CS. Laryngeal tissues were harvested and evaluated using a 254-plex NanoString inflammation panel and neutrophil/macrophage/T-cell immunohistochemistry (IHC). NanoString global and differential gene expression analysis revealed a unique expression profile only in the HD group, with 26 significant differentially expressed genes (DEGs). StringDB KEGG pathway enrichment analysis revealed the involvement of these DEGs with pro-inflammatory pathways including TNF/TNFα and IL-17. Furthermore, inflammatory responses remained inhibited in conjunction with predicted activated states of anti-inflammatory regulators like PPARγ and NFE2L2 upon Ingenuity Pathway Analysis (IPA). Subglottic T-cell levels remained significantly inhibited as corroborated by IPA predictions. Overall, our key findings are consistent with HD exposures being anti-inflammatory and immunosuppressive. Furthermore, the identification of important regulatory genes and enriched pathways may help improve clinical interventions for CS-induced laryngeal diseases.
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Registered trials
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