Clark, Graeme C, Elfsmark, Linda, Armstrong, Stuart ORCID: 0000-0002-3862-1801, Essex-Lopresti, Angela, Gustafsson, Åsa, Ryan, Yan ORCID: 0000-0002-4708-5350, Moore, Karen, Paszkiewicz, Konrad, Green, A Christopher, Hiscox, Julian A ORCID: 0000-0002-6582-0275 et al (show 2 more authors)
(2022)
From "crisis to recovery": A complete insight into the mechanisms of chlorine injury in the lung.
Life sciences, 312.
p. 121252.
Abstract
Chlorine (Cl<sub>2</sub>) gas is a toxic industrial chemical (TIC) that poses a hazard to human health following accidental and/or intentional (e.g. terrorist) release. By using a murine model of sub-lethal Cl<sub>2</sub> exposure we have examined the airway hyper responsiveness, cellular infiltrates, transcriptomic and proteomic responses of the lung. In the "crisis" phase at 2 h and 6 h there is a significant decreases in leukocytes within bronchoalveolar lavage fluid accompanied by an upregulation within the proteome of immune pathways ultimately resulting in neutrophil influx at 24 h. A flip towards "repair" in the transcriptome and proteome occurs at 24 h, neutrophil influx and an associated drop in the lung function persisting until 14 d post-exposure and subsequent "recovery" after 28 days. Collectively, this research provides new insights into the mechanisms of damage, early global responses and processes of repair induced in the lung following the inhalation of Cl<sub>2</sub>.
Item Type: | Article |
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Uncontrolled Keywords: | Chlorine gas, Sub-lethal, Inhalation exposure, Transcriptomics, Proteomics, Lung damage |
Divisions: | Faculty of Health and Life Sciences Faculty of Health and Life Sciences > Institute of Infection, Veterinary and Ecological Sciences |
Depositing User: | Symplectic Admin |
Date Deposited: | 09 Dec 2022 10:47 |
Last Modified: | 20 Jan 2023 05:46 |
DOI: | 10.1016/j.lfs.2022.121252 |
Open Access URL: | https://www.sciencedirect.com/science/article/pii/... |
Related URLs: | |
URI: | https://livrepository.liverpool.ac.uk/id/eprint/3166577 |