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dc.contributor.authorJohnson, Jill R
dc.contributor.authorNishioka, Michiyoshi
dc.contributor.authorChakir, Jamila
dc.contributor.authorRisse, Paul-André
dc.contributor.authorAlmaghlouth, Ibrahim
dc.contributor.authorBazarbashi, Ahmad N
dc.contributor.authorPlante, Sophie
dc.contributor.authorMartin, James G
dc.contributor.authorEidelman, David
dc.contributor.authorHamid, Qutayba
dc.date.accessioned2013-11-12T12:00:53Z
dc.date.available2013-11-12T12:00:53Z
dc.date.issued2013-11-01
dc.identifier.citationRespiratory research. 2013 Nov 01;14(1):118en_GB
dc.identifier.urihttp://dx.doi.org/10.1186/1465-9921-14-118
dc.identifier.urihttp://hdl.handle.net/10147/305239
dc.description.abstractAbstract Background Allergic asthma is characterized by airway inflammation in response to antigen exposure, leading to airway remodeling and lung dysfunction. Epithelial-mesenchymal transition (EMT) may play a role in airway remodeling through the acquisition of a mesenchymal phenotype in airway epithelial cells. TGF-β1 is known to promote EMT; however, other cytokines expressed in severe asthma with extensive remodeling, such as IL-22, may also contribute to this process. In this study, we evaluated the contribution of IL-22 to EMT in primary bronchial epithelial cells from healthy and asthmatic subjects. Methods Primary bronchial epithelial cells were isolated from healthy subjects, mild asthmatics and severe asthmatics (n=5 patients per group). The mRNA and protein expression of epithelial and mesenchymal cell markers and EMT-associated transcription factors was evaluated following stimulation with TGF-β1, IL-22 and TGF-β1+IL-22. Results Primary bronchial epithelial cells stimulated with TGF-β1 underwent EMT, demonstrated by decreased expression of epithelial markers (E-cadherin and MUC5AC) and increased expression of mesenchymal markers (N-cadherin and vimentin) and EMT-associated transcription factors. IL-22 alone had no effect on epithelial or mesenchymal gene expression. However, IL-22+TGF-β1 promoted the expression of some EMT transcription factors (Snail1 and Zeb1) and led to a more profound cadherin shift, but only in cells obtained from severe asthmatics. Conclusion The impact of IL-22 on airway epithelial cells depends on the cytokine milieu and the clinical phenotype of the patient. Further studies are required to determine the molecular mechanism of IL-22 and TGF-β1 cooperativity in driving EMT in primary human bronchial epithelial cells.
dc.language.isoenen
dc.subjectASTHMAen_GB
dc.subjectRESPIRATORY DISORDERen_GB
dc.titleIL-22 contributes to TGF-ß1-mediated epithelial-mesenchymal transition in asthmatic bronchial epithelial cellsen_GB
dc.typeArticleen
dc.identifier.journalRespiratory researchen_GB
dc.language.rfc3066en
dc.rights.holderJill R Johnson et al.; licensee BioMed Central Ltd.
dc.description.statusPeer Reviewed
dc.date.updated2013-11-08T05:15:22Z
refterms.dateFOA2018-08-23T09:38:14Z
html.description.abstractAbstract Background Allergic asthma is characterized by airway inflammation in response to antigen exposure, leading to airway remodeling and lung dysfunction. Epithelial-mesenchymal transition (EMT) may play a role in airway remodeling through the acquisition of a mesenchymal phenotype in airway epithelial cells. TGF-β1 is known to promote EMT; however, other cytokines expressed in severe asthma with extensive remodeling, such as IL-22, may also contribute to this process. In this study, we evaluated the contribution of IL-22 to EMT in primary bronchial epithelial cells from healthy and asthmatic subjects. Methods Primary bronchial epithelial cells were isolated from healthy subjects, mild asthmatics and severe asthmatics (n=5 patients per group). The mRNA and protein expression of epithelial and mesenchymal cell markers and EMT-associated transcription factors was evaluated following stimulation with TGF-β1, IL-22 and TGF-β1+IL-22. Results Primary bronchial epithelial cells stimulated with TGF-β1 underwent EMT, demonstrated by decreased expression of epithelial markers (E-cadherin and MUC5AC) and increased expression of mesenchymal markers (N-cadherin and vimentin) and EMT-associated transcription factors. IL-22 alone had no effect on epithelial or mesenchymal gene expression. However, IL-22+TGF-β1 promoted the expression of some EMT transcription factors (Snail1 and Zeb1) and led to a more profound cadherin shift, but only in cells obtained from severe asthmatics. Conclusion The impact of IL-22 on airway epithelial cells depends on the cytokine milieu and the clinical phenotype of the patient. Further studies are required to determine the molecular mechanism of IL-22 and TGF-β1 cooperativity in driving EMT in primary human bronchial epithelial cells.


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