دورية أكاديمية

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

التفاصيل البيبلوغرافية
العنوان: Azithromycin ameliorates sulfur dioxide-induced airway epithelial damage and inflammatory responses.
المؤلفون: Joelsson, Jon Petur, Kricker, Jennifer A, Arason, Ari J, Sigurdsson, Snaevar, Valdimarsdottir, Bryndis, Gardarsson, Fridrik Runar, Page, Clive P, Lehmann, Fredrik, Gudjonsson, Thorarinn, Ingthorsson, Saevar
المساهمون: 1Stem Cell Research Unit, BioMedical Center, School of Health Sciences, University of Iceland, Reykjavík, Iceland. 2EpiEndo Pharmaceuticals, Reykjavík, Iceland. 3Department of Laboratory Hematology, Landspitali-University Hospital, Reykjavík, Iceland. 4Biomedical Center, University of Iceland, Reykjavík, Iceland. 5Sackler Institute of Pulmonary Pharmacology, King's College London, London, UK. 6Stem Cell Research Unit, BioMedical Center, School of Health Sciences, University of Iceland, Reykjavík, Iceland. saevari@hi.is. 7EpiEndo Pharmaceuticals, Reykjavík, Iceland. saevari@hi.is. 8Faculty of Nursing, University of Iceland, Reykjavík, Iceland. saevari@hi.is.
المصدر: Respiratory research ; 21 ; 1 ; 233 ; England
بيانات النشر: BioMed Central
سنة النشر: 2020
المجموعة: Hirsla - Landspítali University Hospital research archive
مصطلحات موضوعية: Azithromycin, Glutathione-S-transferase, Immunomodulation, Lamellar bodies, Lung barrier enhancement, Lungnasjúkdómar, Lyfjagjöf, Lyf, Lung Diseases, Drug Therapy
الوصف: To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Download ; 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. Keywords: Azithromycin; Glutathione-S-transferase; Immunomodulation; Lamellar bodies; Lung barrier enhancement. ; Icelandic Research Council Technical Fund (Rannis Grant) EpiEndo Pharmaceuticals
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 1465-993X
العلاقة: https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-020-01489-8Test; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7488110Test/; Joelsson JP, Kricker JA, Arason AJ, Sigurdsson S, Valdimarsdottir B, Gardarsson FR, Page CP, Lehmann F, Gudjonsson T, Ingthorsson S. Azithromycin ameliorates sulfur dioxide-induced airway epithelial damage and inflammatory responses. Respir Res. 2020 Sep 10;21(1):233. doi:10.1186/s12931-020-01489-8; http://hdl.handle.net/2336/621567Test; Respiratory research
DOI: 10.1186/s12931-020-01489-8
الإتاحة: https://doi.org/10.1186/s12931-020-01489-8Test
http://hdl.handle.net/2336/621567Test
حقوق: Open Access - Opinn aðgangur
رقم الانضمام: edsbas.57A62EF5
قاعدة البيانات: BASE
الوصف
تدمد:1465993X
DOI:10.1186/s12931-020-01489-8