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Azithromycin ameliorates sulfur dioxide-induced airway epithelial damage and inflammatory responses

Azithromycin ameliorates sulfur dioxide-induced airway epithelial damage and inflammatory responses

Title: Azithromycin ameliorates sulfur dioxide-induced airway epithelial damage and inflammatory responses
Author: Jóelsson, Jón Pétur
Kricker, Jennifer   orcid.org/0000-0002-0757-1936
Arason, Ari Jon   orcid.org/0000-0003-0252-7992
Sigurdsson, Snaevar   orcid.org/0000-0003-4860-6311
Valdimarsdóttir, Bryndís
Garðarsson, Friðrik Rúnar
Page, Clive P.
Lehmann, Fredrik
Gudjonsson, Thorarinn   orcid.org/0000-0001-9645-9665
Ingthorsson, Saevar   orcid.org/0000-0001-8480-9680
Date: 2020-09-10
Language: English
Scope: 233
University/Institute: Háskóli Íslands
University of Iceland
School: Heilbrigðisvísindasvið (HÍ)
School of Health Sciences (UI)
Department: Lífvísindasetur (HÍ)
Biomedical Center (UI)
Hjúkrunarfræðideild (HÍ)
Faculty of Nursing (UI)
Series: Respiratory Research;21(1)
ISSN: 1465-993X
DOI: 10.1186/s12931-020-01489-8
Subject: Azithromycin; Glutathione-S-transferase; Immunomodulation; Lamellar bodies; Lung barrier enhancement; Bólgur; Brennisteinsdíoxíð; Lungu; Öndunarfærasjúkdómar
URI: https://hdl.handle.net/20.500.11815/2199

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Joelsson, J.P., Kricker, J.A., Arason, A.J. et al. Azithromycin ameliorates sulfur dioxide-induced airway epithelial damage and inflammatory responses. Respiratory Research 21, 233 (2020). https://doi.org/10.1186/s12931-020-01489-8


Background: The airway epithelium (AE) forms the first line of defence against harmful particles and pathogens. Barrier failure of the airway epithelium contributes to exacerbations of a range of lung diseases that are commonly treated with Azithromycin (AZM). In addition to its anti-bacterial function, AZM has immunomodulatory effects which are proposed to contribute to its clinical effectiveness. In vitro studies have shown the AE barrier-enhancing effects of AZM. The aim of this study was to analyze whether AE damage caused by inhalation of sulfur dioxide (SO2) in a murine model could be reduced by pre-treatment with AZM. Methods: The leakiness of the AE barrier was evaluated after SO2 exposure by measuring levels of human serum albumin (HSA) in bronchoalveolar lavage fluid (BALF). Protein composition in BALF was also assessed and lung tissues were evaluated across treatments using histology and gene expression analysis. Results: AZM pre-treatment (2 mg/kg p.o. 5 times/week for 2 weeks) resulted in reduced glutathione-S-transferases in BALF of SO2 injured mice compared to control (without AZM treatment). AZM treated mice had increased intracellular vacuolization including lamellar bodies and a reduction in epithelial shedding after injury in addition to a dampened SO2-induced inflammatory response. Conclusions: Using a mouse model of AE barrier dysfunction we provide evidence for the protective effects of AZM in vivo, possibly through stabilizing the intracellular microenvironment and reducing inflammatory responses. Our data provide insight into the mechanisms contributing to the efficacy of AZM in the treatment of airway diseases.


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