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Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy

PURPOSE: Tuberculous pleurisy is the most frequent extrapulmonary manifestation of tuberculosis. In spite of adequate treatment, pleural fibrosis is a common complication, but the mechanism has not been elucidated. This study is to determine whether epithelial to mesenchymal transition (EMT) of meso...

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Autores principales: Kim, Changhwan, Kim, Dong-Gyu, Park, Sung-Hoon, Hwang, Yong Il, Jang, Seung Hun, Kim, Cheol Hong, Jung, Ki-Suck, Min, Kwangseon, Lee, Jae Woong, Jang, Young Sook
Formato: Texto
Lenguaje:English
Publicado: Yonsei University College of Medicine 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017708/
https://www.ncbi.nlm.nih.gov/pubmed/21155035
http://dx.doi.org/10.3349/ymj.2011.52.1.51
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author Kim, Changhwan
Kim, Dong-Gyu
Park, Sung-Hoon
Hwang, Yong Il
Jang, Seung Hun
Kim, Cheol Hong
Jung, Ki-Suck
Min, Kwangseon
Lee, Jae Woong
Jang, Young Sook
author_facet Kim, Changhwan
Kim, Dong-Gyu
Park, Sung-Hoon
Hwang, Yong Il
Jang, Seung Hun
Kim, Cheol Hong
Jung, Ki-Suck
Min, Kwangseon
Lee, Jae Woong
Jang, Young Sook
author_sort Kim, Changhwan
collection PubMed
description PURPOSE: Tuberculous pleurisy is the most frequent extrapulmonary manifestation of tuberculosis. In spite of adequate treatment, pleural fibrosis is a common complication, but the mechanism has not been elucidated. This study is to determine whether epithelial to mesenchymal transition (EMT) of mesothelial cells occurs in tuberculous pleurisy. MATERIALS AND METHODS: Normal pleural mesothelial cells, isolated from irrigation fluids during operations for primary spontaneous pneumothorax, were characterized by immunofluorescence and reverse transcription polymerase chain reaction (RT-PCR). These cells were treated in vitro with various cytokines, which were produced in the effluents of tuberculous pleurisy. The isolated cells from the effluents of tuberculous pleurisy were analyzed by immunofluorescence and RT-PCR analysis. RESULTS: The isolated cells from the irrigation fluid of primary spontaneous pneumothorax had epithelial characteristics. These cells, with transforming growth factor-β1 and/or interleukin-1β treatment, underwent phenotypic transition from epithelial to mesenchymal cells, with the loss of epithelial morphology and reduction in cytokeratin and E-cadherin expression. Effluent analysis from tuberculous pleurisy using immunofluorescence and RT-PCR demonstrated two phenotypes that showed mesenchymal characteristics and both epithelial & mesencymal characteristics. CONCLUSION: Our results suggest that pleural mesothelial cells in tuberculous pleurisy have been implicated in pleural fibrosis through EMT.
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spelling pubmed-30177082011-01-10 Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy Kim, Changhwan Kim, Dong-Gyu Park, Sung-Hoon Hwang, Yong Il Jang, Seung Hun Kim, Cheol Hong Jung, Ki-Suck Min, Kwangseon Lee, Jae Woong Jang, Young Sook Yonsei Med J Original Article PURPOSE: Tuberculous pleurisy is the most frequent extrapulmonary manifestation of tuberculosis. In spite of adequate treatment, pleural fibrosis is a common complication, but the mechanism has not been elucidated. This study is to determine whether epithelial to mesenchymal transition (EMT) of mesothelial cells occurs in tuberculous pleurisy. MATERIALS AND METHODS: Normal pleural mesothelial cells, isolated from irrigation fluids during operations for primary spontaneous pneumothorax, were characterized by immunofluorescence and reverse transcription polymerase chain reaction (RT-PCR). These cells were treated in vitro with various cytokines, which were produced in the effluents of tuberculous pleurisy. The isolated cells from the effluents of tuberculous pleurisy were analyzed by immunofluorescence and RT-PCR analysis. RESULTS: The isolated cells from the irrigation fluid of primary spontaneous pneumothorax had epithelial characteristics. These cells, with transforming growth factor-β1 and/or interleukin-1β treatment, underwent phenotypic transition from epithelial to mesenchymal cells, with the loss of epithelial morphology and reduction in cytokeratin and E-cadherin expression. Effluent analysis from tuberculous pleurisy using immunofluorescence and RT-PCR demonstrated two phenotypes that showed mesenchymal characteristics and both epithelial & mesencymal characteristics. CONCLUSION: Our results suggest that pleural mesothelial cells in tuberculous pleurisy have been implicated in pleural fibrosis through EMT. Yonsei University College of Medicine 2011-01-01 2010-11-30 /pmc/articles/PMC3017708/ /pubmed/21155035 http://dx.doi.org/10.3349/ymj.2011.52.1.51 Text en © Copyright: Yonsei University College of Medicine 2011 http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Kim, Changhwan
Kim, Dong-Gyu
Park, Sung-Hoon
Hwang, Yong Il
Jang, Seung Hun
Kim, Cheol Hong
Jung, Ki-Suck
Min, Kwangseon
Lee, Jae Woong
Jang, Young Sook
Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy
title Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy
title_full Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy
title_fullStr Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy
title_full_unstemmed Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy
title_short Epithelial to Mesenchymal Transition of Mesothelial Cells in Tuberculous Pleurisy
title_sort epithelial to mesenchymal transition of mesothelial cells in tuberculous pleurisy
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017708/
https://www.ncbi.nlm.nih.gov/pubmed/21155035
http://dx.doi.org/10.3349/ymj.2011.52.1.51
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