Heat shock protein (HSP 70) expression in septic patients

Purpose : This study investigates heat shock protein 70 (HSP 70) expression by peripheral blood mononuclear cells (PBMCs) of septic patients admitted to an intensive care unit and examines the possibility of a correlation between HSP 70 levels and plasma tumor necrosis factor alpha (TNF-α) concentra...

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Bibliographic Details
Published in:Journal of critical care Vol. 12; no. 4; pp. 188 - 192
Main Authors: Delogu, Giovanna, Lo Bosco, Livia, Marandola, Maurizio, Famularo, Giuseppe, Lenti, Luisa, Ippoliti, Flora, Signore, Luciano
Format: Journal Article
Language:English
Published: United States Elsevier Inc 01-12-1997
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Summary:Purpose : This study investigates heat shock protein 70 (HSP 70) expression by peripheral blood mononuclear cells (PBMCs) of septic patients admitted to an intensive care unit and examines the possibility of a correlation between HSP 70 levels and plasma tumor necrosis factor alpha (TNF-α) concentrations. Additionally, we evaluated whether the HSP 70 production could be regarded as a prognostic factor for the development of septic shock as well as for patient survival. Materials and Methods : Blood samples of 29 patients were taken 24 hours after the diagnosis of sepsis. HSP 70 expression and TNF-α level were measured using indirect immunofluorescent analysis and a commercially available enzyme-linked immunosorbent assay method, respectively. Results : PBMCs expressed significantly high levels of HSP 70 (11.9 ± 5.6 [sd]) compared with those of the healthy control group (3.2 ± 2.1 % positive cells). Such enhanced levels were correlated to plasma TNF-α concentrations ( r = .99, P < .01). This study failed to demonstrate a relationship between HSP 70 production and clinical outcome. Conclusion : These findings give further evidence that also in humans, heat shock response is activated during sepsis. The correlation observed between HSP 70 overproduction and TNF-α plasma concentrations suggests that HSP 70 exerts a possible protective effect against TNF-α cytotoxicity. Such hypothesis has not been confirmed by our clinical data.
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ISSN:0883-9441
1557-8615
DOI:10.1016/S0883-9441(97)90031-9