Viral infection drives tissue fibrosis in vitro
Idiopathic Pulmonary Fibrosis (IPF) is a refractory and lethal interstitial lung disease characterized by loss of alveolar epithelial cells, fibroblast proliferation and extra-cellular matrix protein deposition. EBV, localised to alveolar epithelial cells of pulmonary fibrosis patients is associated...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Respiratory Society
2008-04-01
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| Series: | European Respiratory Review |
| Online Access: | http://err.ersjournals.com/cgi/content/full/17/107/49 |
| _version_ | 1819042219361828864 |
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| author | Andrea P. Malizia Dermot Walls Jim J. Egan Peter P. Doran |
| author_facet | Andrea P. Malizia Dermot Walls Jim J. Egan Peter P. Doran |
| author_sort | Andrea P. Malizia |
| collection | DOAJ |
| description | Idiopathic Pulmonary Fibrosis (IPF) is a refractory and lethal interstitial lung disease characterized by loss of alveolar epithelial cells, fibroblast proliferation and extra-cellular matrix protein deposition. EBV, localised to alveolar epithelial cells of pulmonary fibrosis patients is associated with a poor prognosis. In this study we utilised a microarray-based differential gene expression analysis strategy to identify molecular drivers of EBV associated with lung fibrosis. A549 cells and an alveolar epithelial cell line infected with EBV (VAAK) were used to identify genes whose expression was altered by EBV reactivation. EBV reactivation by TGFbeta1 drives alterations in expression of non-canonical Wnt pathway mediators, implicating it in epithelial mesenchymal transition (EMT), the molecular event underpinning scar production in tissue fibrosis. Cell invasion, EMT correlated transcripts expression, GSK-3b and c-Jun activation were altered in response to non-canonical Wnt pathway regulation. The role of EBV in promoting fibrosis can be attenuated by antiviral strategies and inhibition of Wnt signalling. Activation of non-canonical Wnt signalling pathway by EBV in epithelial cells suggests a novel mechanism of tissue fibrosis. These data present a framework for further description of the link between infectious agents and fibrosis, a significant disease burden. |
| first_indexed | 2024-12-21T09:37:25Z |
| format | Article |
| id | doaj.art-067dcf490004484cb66114e3e1dd58e7 |
| institution | Directory Open Access Journal |
| issn | 0905-9180 1600-0617 |
| language | English |
| last_indexed | 2024-12-21T09:37:25Z |
| publishDate | 2008-04-01 |
| publisher | European Respiratory Society |
| record_format | Article |
| series | European Respiratory Review |
| spelling | doaj.art-067dcf490004484cb66114e3e1dd58e72022-12-21T19:08:35ZengEuropean Respiratory SocietyEuropean Respiratory Review0905-91801600-06172008-04-01171074950Viral infection drives tissue fibrosis in vitroAndrea P. MaliziaDermot WallsJim J. EganPeter P. DoranIdiopathic Pulmonary Fibrosis (IPF) is a refractory and lethal interstitial lung disease characterized by loss of alveolar epithelial cells, fibroblast proliferation and extra-cellular matrix protein deposition. EBV, localised to alveolar epithelial cells of pulmonary fibrosis patients is associated with a poor prognosis. In this study we utilised a microarray-based differential gene expression analysis strategy to identify molecular drivers of EBV associated with lung fibrosis. A549 cells and an alveolar epithelial cell line infected with EBV (VAAK) were used to identify genes whose expression was altered by EBV reactivation. EBV reactivation by TGFbeta1 drives alterations in expression of non-canonical Wnt pathway mediators, implicating it in epithelial mesenchymal transition (EMT), the molecular event underpinning scar production in tissue fibrosis. Cell invasion, EMT correlated transcripts expression, GSK-3b and c-Jun activation were altered in response to non-canonical Wnt pathway regulation. The role of EBV in promoting fibrosis can be attenuated by antiviral strategies and inhibition of Wnt signalling. Activation of non-canonical Wnt signalling pathway by EBV in epithelial cells suggests a novel mechanism of tissue fibrosis. These data present a framework for further description of the link between infectious agents and fibrosis, a significant disease burden.http://err.ersjournals.com/cgi/content/full/17/107/49 |
| spellingShingle | Andrea P. Malizia Dermot Walls Jim J. Egan Peter P. Doran Viral infection drives tissue fibrosis in vitro European Respiratory Review |
| title | Viral infection drives tissue fibrosis in vitro |
| title_full | Viral infection drives tissue fibrosis in vitro |
| title_fullStr | Viral infection drives tissue fibrosis in vitro |
| title_full_unstemmed | Viral infection drives tissue fibrosis in vitro |
| title_short | Viral infection drives tissue fibrosis in vitro |
| title_sort | viral infection drives tissue fibrosis in vitro |
| url | http://err.ersjournals.com/cgi/content/full/17/107/49 |
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