ArticleJournal of Korean medical science2020
Effects of Ammonium Chloride on Ozone-induced Airway Inflammation: the Role of Slc26a4 in the Lungs of Mice.
Article in Journal of Korean medical science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Article
- Establishment of an artificial particulate matter-induced lung disease model through analyzing pathological changes and transcriptomic profiles in mice.Scientific reports · 2023Article
- Function-specific IL-17A and dexamethasone interactions in primary human airway epithelial cells.Scientific reports · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundExposure to ozone (O₃) induces neutrophilic inflammation and goblet cell hyperplasia in humans and experimental animals. Because the solute carrier family 26-member 4 (Slc26a4; pendrin) gene induces mucin production and intraluminal acidification in the airways, it was hypothesized to be a key molecule in O₃-induced airway injury. Thus, we evaluated the role of Slc26a4 and the protective effects of ammonium chloride (NH₄Cl) in O₃-induced airway injury in mice.
methodsSix-week-old female BALB/c mice were exposed to filtered air or O₃ for 21 days (2 ppm for 3 hr/day). NH₄Cl (0, 0.1, 1, and 10 mM) was administered intratracheally into the airways. Airway resistance was measured using a flexiVent system, and bronchoalveolar lavage fluid (BALF) cells were differentially counted. Slc26a4 and Muc5ac proteins and mRNA were measured via western blotting, real-time polymerase chain reaction, and immunostaining. Tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-17, IL-1β, and caspase-1 were analyzed via western blotting.
resultsThe levels Slc26a4 protein and mRNA significantly increased in lung tissues from Day 7 to Day 21 of O₃ exposure, with concomitant increases in lung resistance, numbers of goblet cells in lung tissues, and inflammatory cells and thiocyanate (SCN
conclusionSlc26a4 may be involved in O₃-induced inflammatory and epithelial changes in the airways via activation of the inflammasome and the induction of IL-17 and IFN-γ. NH₄Cl shows a potential as a therapeutic agent for controlling O₃-induced airway inflammation and epithelial damage by modulating Slc26a4 expression.
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