Abstract
Objective. We assessed the lipopolysaccharide (LPS) or heat shock (HS) induction of heat shock protein-72 (HSP72) in peripheral blood mononuclear cells (PBMCs) of patients with severe sepsis (SS) or trauma-related systemic inflammatory response syndrome (SIRS), compared to healthy individuals (H); we also investigated any pre- or posttreatment modulating glutamine (Gln) effect. Methods. SS (11), SIRS (10), and H (19) PBMCs were incubated with 1 μg/mL LPS or 43°HS. Gln 10 mM was either added 1 h before or 1 h after induction or was not added at all. We measured monocyte (m), lymphocyte (l), mRNA HSP72, HSP72 polymorphisms, interleukins (ILs), monocyte chemoattractant protein-1 (MCP-1), and cortisol levels. Results. Baseline lHSP72 was higher in SS (p < 0.03), and mHSP72 in SIRS (p < 0.02), compared to H. Only HS induced l/mHSP72/mRNA HSP72; LPS induced IL-6, IL-8, IL-10, and MCP-1. Induced mRNA was related to l/mHSP72, and was related negatively to cytokines. Intracellular l/mHSP72/HSP72 mRNA was related to serum ILs, not being influenced by cortisol, illness severity, and HSP72 polymorphisms. Gln did not induce mRNA in any group but modified l/mHSP72 after LPS/HS induction unpredictably. Conclusions. HSP72 mRNA and l/mHSP72 are higher among critically ill patients, further induced by HS, not by LPS. HSP72 proteins and HSP72 mRNA are related to serum ILs and are negatively related to supernatant cytokines, not being influenced by HSP72 polymorphisms, cortisol, or illness severity. Gln may depress l/mHSP72 after LPS exposure and enhance them after HS induction, but it may not affect early induced HSP72 mRNA.
Highlights
Fever commonly characterizes the infectious or noninfectious systemic inflammatory response syndrome (SIRS) [1]
Baseline mHSP72 was higher in SS and SIRS compared to H (Mann-Whitney U tests), and lHSP72 was higher in SS compared to H (Figure 1)
We present here the first study to show that intracellular monocyte or lymphocyte heat shock protein-72 (HSP72) protein expression and HSP72 mRNA are higher in intensive care unit (ICU) patients with septic shock/severe sepsis or with trauma compared to healthy individuals
Summary
Fever commonly characterizes the infectious or noninfectious systemic inflammatory response syndrome (SIRS) [1]. There may be a relationship between elevated early peak temperature and decreased mortality at 28 days [2] or hospital discharge [3]. SIRS, high fever (>38∘C) and fever burden in the first 72 h are associated with an increase in mortality [4]. Fever treatment of influenza infection has been reported to be associated with mortality [5]. In intensive care unit (ICU) patients without acute neurological injury, no association between antipyretics and mortality could be found [6]
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