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Published on: August 19, 2016
Bacterial infection elicits heat shock protein 72 release from pleural mesothelial cells
Julius F Varano Della Vergiliana1, Sally M Lansley, Jose M Porcel
1Pleural Disease Unit, Lung Institute of Western Australia, Centre for Asthma, Allergy and Respiratory Research, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia.
Abstract:
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.
Insights
Pleural mesothelial cells release Heat Shock Protein 70 (HSP70), specifically Hsp72, when exposed to bacterial infection. Elevated Hsp72 levels in pleural effusions may aid in diagnosing infectious conditions.
Area of Science:
- Immunology
- Cell Biology
- Infectious Diseases
Background:
- Heat shock protein 70 (HSP70) is involved in infection responses and detected in bodily fluids during infection.
- Pleural mesothelial cells play a role in serosal infections.
Purpose of the Study:
- To investigate if pleural mesothelial cells release HSP70 in response to bacterial infection.
- To examine the in vitro effects of Hsp72 on mesothelial cells.
- To evaluate Hsp72 as a diagnostic marker for infectious pleural effusions.
Main Methods:
- In vitro stimulation of mesothelial cells with Streptococcus pneumoniae.
- Induction of bacterial peritonitis in mouse models.
- Measurement of Hsp72 in peritoneal lavage fluid and human pleural effusions.
- Comparison of Hsp72 levels in infectious vs. non-infectious effusions.
Main Results:
- Mesothelial cells significantly increased Hsp72 release upon exposure to S. pneumoniae.
- S. pneumoniae infection in mice led to a 2-fold increase in peritoneal lavage Hsp72.
- Extracellular Hsp72 did not modulate mediator release from mesothelial cells.
- Hsp72 levels were significantly higher in infectious pleural effusions compared to non-infectious ones.
Conclusions:
- Pleural mesothelial cells are a source of Hsp72 during bacterial infection.
- Elevated Hsp72 in pleural effusions suggests potential diagnostic utility for infection.
- Further research is needed to elucidate the role of HSP70 in pleural infections.
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