Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.

Heat shock protein 70 (HSP70) has been implicated in infection-related processes and has been found in body fluids during infection. This study aimed to determine whether pleural mesothelial cells release HSP70 in response to bacterial infection in vitro and in mouse models of serosal infection. In...

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Autores principales:	Julius F Varano Della Vergiliana, Sally M Lansley, Jose M Porcel, Silvia Bielsa, Jeremy S Brown, Jenette Creaney, Suzanna E L Temple, Grant W Waterer, Y C Gary Lee
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c2893851451f4837807869d8638a5c00
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spelling	oai:doaj.org-article:c2893851451f4837807869d8638a5c002021-11-18T07:44:53ZBacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.1932-620310.1371/journal.pone.0063873https://doaj.org/article/c2893851451f4837807869d8638a5c002013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23704948/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Heat shock protein 70 (HSP70) has been implicated in infection-related processes and has been found in body fluids during infection. This study aimed to determine whether pleural mesothelial cells release HSP70 in response to bacterial infection in vitro and in mouse models of serosal infection. In addition, the in vitro cytokine effects of the HSP70 isoform, Hsp72, on mesothelial cells were examined. Further, Hsp72 was measured in human pleural effusions and levels compared between non-infectious and infectious patients to determine the diagnostic accuracy of pleural fluid Hsp72 compared to traditional pleural fluid parameters. We showed that mesothelial release of Hsp72 was significantly raised when cells were treated with live and heat-killed Streptococcus pneumoniae. In mice, intraperitoneal injection of S. pneumoniae stimulated a 2-fold increase in Hsp72 levels in peritoneal lavage (p<0.01). Extracellular Hsp72 did not induce or inhibit mediator release from cultured mesothelial cells. Hsp72 levels were significantly higher in effusions of infectious origin compared to non-infectious effusions (p<0.05). The data establish that pleural mesothelial cells can release Hsp72 in response to bacterial infection and levels are raised in infectious pleural effusions. The biological role of HSP70 in pleural infection warrants exploration.Julius F Varano Della VergilianaSally M LansleyJose M PorcelSilvia BielsaJeremy S BrownJenette CreaneySuzanna E L TempleGrant W WatererY C Gary LeePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 5, p e63873 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Julius F Varano Della Vergiliana Sally M Lansley Jose M Porcel Silvia Bielsa Jeremy S Brown Jenette Creaney Suzanna E L Temple Grant W Waterer Y C Gary Lee Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
description	Heat shock protein 70 (HSP70) has been implicated in infection-related processes and has been found in body fluids during infection. This study aimed to determine whether pleural mesothelial cells release HSP70 in response to bacterial infection in vitro and in mouse models of serosal infection. In addition, the in vitro cytokine effects of the HSP70 isoform, Hsp72, on mesothelial cells were examined. Further, Hsp72 was measured in human pleural effusions and levels compared between non-infectious and infectious patients to determine the diagnostic accuracy of pleural fluid Hsp72 compared to traditional pleural fluid parameters. We showed that mesothelial release of Hsp72 was significantly raised when cells were treated with live and heat-killed Streptococcus pneumoniae. In mice, intraperitoneal injection of S. pneumoniae stimulated a 2-fold increase in Hsp72 levels in peritoneal lavage (p<0.01). Extracellular Hsp72 did not induce or inhibit mediator release from cultured mesothelial cells. Hsp72 levels were significantly higher in effusions of infectious origin compared to non-infectious effusions (p<0.05). The data establish that pleural mesothelial cells can release Hsp72 in response to bacterial infection and levels are raised in infectious pleural effusions. The biological role of HSP70 in pleural infection warrants exploration.
format	article
author	Julius F Varano Della Vergiliana Sally M Lansley Jose M Porcel Silvia Bielsa Jeremy S Brown Jenette Creaney Suzanna E L Temple Grant W Waterer Y C Gary Lee
author_facet	Julius F Varano Della Vergiliana Sally M Lansley Jose M Porcel Silvia Bielsa Jeremy S Brown Jenette Creaney Suzanna E L Temple Grant W Waterer Y C Gary Lee
author_sort	Julius F Varano Della Vergiliana
title	Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
title_short	Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
title_full	Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
title_fullStr	Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
title_full_unstemmed	Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
title_sort	bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/c2893851451f4837807869d8638a5c00
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Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.

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