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

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2013Author
Varano della Vergiliana, Julius F.
Lansley, Sally M.
Brown, Jeremy S.
Creaney, Jenette
Temple, Suzanna E. L.
Waterer, Grant W.
Gary Lee, Y. C.
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Varano della Vergiliana, Julius F.;
Lansley, Sally M.;
Porcel Pérez, José Manuel;
Bielsa Martín, Silvia;
Brown, Jeremy S.;
Creaney, Jenette;
...
Gary Lee, Y. C..
(2013)
.
Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells.
PLoS One, 2013, vol. 8, núm. 5, e63873.
https://doi.org/10.1371/journal.pone.0063873.
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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.
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PLoS One, 2013, vol. 8, núm. 5, e63873European research projects
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