ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Abnormal epithelial structure and chronic lung inflammation after repair of chlorine-induced airway injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- A human airway-on-a-chip microphysiological system for modeling chlorine gas toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Countermeasures against Pulmonary Threat Agents.The Journal of pharmacology and experimental therapeutics · 2024Review
- Leukotriene BBiomedicines · 2022Article
- MMP-3 activation is involved in copper oxide nanoparticle-induced epithelial-mesenchymal transition in human lung epithelial cells.Nanotoxicology · 2021Article
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions.PLoS pathogens · 2021Article
- Toxic effects of chlorine gas and potential treatments: a literature review.Toxicology mechanisms and methods · 2021Review
- Effects of metal nanoparticles on tight junction-associated proteins via HIF-1α/miR-29b/MMPs pathway in human epidermal keratinocytes.Particle and fibre toxicology · 2021Article
- Transient receptor potential channels in pulmonary chemical injuries and as countermeasure targets.Annals of the New York Academy of Sciences · 2020Article
- Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020Review
- Disease-modifying treatment of chemical threat agent-induced acute lung injury.Annals of the New York Academy of Sciences · 2020Review
- miR-21 mediates nickel nanoparticle-induced pulmonary injury and fibrosis.Nanotoxicology · 2020Article
- Inhibition of chlorine-induced airway fibrosis by budesonide.Toxicology and applied pharmacology · 2019Article
- Comparative mouse lung injury by nickel nanoparticles with differential surface modification.Journal of nanobiotechnology · 2019Article
- Granulocyte-CSF links destructive inflammation and comorbidities in obstructive lung disease.The Journal of clinical investigation · 2018Article
- Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse.British journal of pharmacology · 2017Article
- Persistent effects of chlorine inhalation on respiratory health.Annals of the New York Academy of Sciences · 2016Review
- Lung Function before and after a Large Chlorine Gas Release in Graniteville, South Carolina.Annals of the American Thoracic Society · 2016Article
- Heme Attenuation Ameliorates Irritant Gas Inhalation-Induced Acute Lung Injury.Antioxidants & redox signaling · 2016Article
- Respiratory syncytial virus infection increases chlorine-induced airway hyperresponsiveness.American journal of physiology. Lung cellular and molecular physiology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Chlorine is a toxic gas used in a variety of industrial processes and is considered a chemical threat agent. High-level chlorine exposure causes acute lung injury, but the long-term effects of acute chlorine exposure are unclear. Here we characterized chronic pulmonary changes following acute chlorine exposure in mice. A/J mice were exposed to 240 parts per million-hour chlorine or sham-exposed to air. Chlorine inhalation caused sloughing of bronchial epithelium 1 day after chlorine exposure, which was repaired with restoration of a pseudostratified epithelium by day 7. The repaired epithelium contained an abnormal distribution of epithelial cells containing clusters of club or ciliated cells rather than the uniformly interspersed pattern of these cells in unexposed mice. Although the damaged epithelium in A/J mice was repaired rapidly, and minimal airway fibrosis was observed, chlorine-exposed mice developed pneumonitis characterized by infiltration of alveoli with neutrophils and prominent, large, foamy macrophages. Levels of CXCL1/KC, CXCL5/LPS-induced CXC chemokine, granulocyte colony-stimulating factor, and VEGF in bronchoalveolar (BAL) fluid from chlorine-exposed mice showed steadily increasing trends over time. BAL protein levels were increased on day 4 and remained elevated out to day 28. The number of bacteria cultured from lungs of chlorine-exposed mice 4 wk after exposure was not increased compared with sham-exposed mice, indicating that the observed pneumonitis was not driven by bacterial infection of the lung. The results indicate that acute chlorine exposure may cause chronic abnormalities in the lungs despite rapid repair of injured epithelium.
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Registered trials
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