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dc.contributor.authorRoberts, Nicole
dc.contributor.authorAl Mubarak, Reem
dc.contributor.authorFrancisco, David
dc.contributor.authorKraft, Monica
dc.contributor.authorChu, Hong Wei
dc.date.accessioned2018-06-04T23:30:41Z
dc.date.available2018-06-04T23:30:41Z
dc.date.issued2018-05-02
dc.identifier.citationRoberts, N., Al Mubarak, R., Francisco, D., Kraft, M., & Chu, H. W. (2018). Comparison of paired human nasal and bronchial airway epithelial cell responses to rhinovirus infection and IL-13 treatment. Clinical and translational medicine, 7(1), 13.en_US
dc.identifier.issn2001-1326
dc.identifier.pmid29721720
dc.identifier.doi10.1186/s40169-018-0189-2
dc.identifier.urihttp://hdl.handle.net/10150/627881
dc.description.abstractBackground: Because of its advantage as a minimally invasive procedure, nasal brushings have been increasingly used and proposed as a valuable approach to study lower airway diseases in lieu of bronchial epithelial cells. However, there is limited or conflicting evidence pertaining to whether nasal samples can be surrogates to bronchial samples. The goal of the present study is to test whether nasal epithelial cells have similar antiviral and inflammatory responses to IL-13 treatment and rhinovirus infection, a condition mimicking virally induced asthma exacerbation. Nasal and bronchial airway epithelial cells taken from the same patient were cultured under submerged and air-liquid interface (ALI) culture in the absence or presence of rhinovirus and IL-13 treatment. Inflammatory cytokines IP-10 and eotaxin-3, antiviral gene Mx1 and viral levels were measured. Results: In the absence of IL-13 treatment, nasal and bronchial cells showed a similar IP-10 response in both ALI and submerged cultures. Under the ALI culture, short term (e.g., 3 days) IL-13 treatment had a minimal effect on viral and Mx1 levels in both cell types. However, prolonged (e.g., 14 days) IL-13 treatments in both cell types decreased viral load and Mx1 expression. Under the submerged culture, IL-13 treatment in both cell types has minimal effects on viral load, IP-10 and Mx1. IL-13-induced eotaxin-3 production was similar in both types of cells under either submerged or ALI culture, which was not affected by viral infection. Conclusions: Our data suggest that nasal epithelial cells could serve as a surrogate to bronchial epithelial cells in future studies aimed at defining the role of type 2 cytokine IL-13 in regulating pro-inflammatory and antiviral responses.en_US
dc.description.sponsorship[U19AI125357]; [R01 HL122321]; [R01 AI106287]; [R01 HL125128]en_US
dc.language.isoenen_US
dc.publisherBIOMED CENTRAL LTDen_US
dc.relation.urlhttps://clintransmed.springeropen.com/articles/10.1186/s40169-018-0189-2en_US
dc.rights© The Author(s) 2018. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectEpithelial cellsen_US
dc.subjectRhinovirusen_US
dc.subjectIL-13en_US
dc.subjectIP-10en_US
dc.subjectEotaxinen_US
dc.titleComparison of paired human nasal and bronchial airway epithelial cell responses to rhinovirus infection and IL-13 treatmenten_US
dc.typeArticleen_US
dc.contributor.departmentUniv Arizona, Dept Meden_US
dc.identifier.journalCLINICAL AND TRANSLATIONAL MEDICINEen_US
dc.description.noteOpen access journal.en_US
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en_US
dc.eprint.versionFinal published versionen_US
dc.source.journaltitleClinical and Translational Medicine
dc.source.volume7
dc.source.issue1
refterms.dateFOA2018-06-04T23:30:41Z


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© The Author(s) 2018. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.
Except where otherwise noted, this item's license is described as © The Author(s) 2018. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.