Περίληψη:
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 g/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. © 2015 Efrossini Briassouli et al.
Συγγραφείς:
Briassouli, E.
Tzanoudaki, M.
Goukos, D.
Routsi, C.
Nanas, S.
Vardas, K.
Apostolou, K.
Kanariou, M.
Daikos, G.
Briassoulis, G.
Λέξεις-κλειδιά:
glutamine; heat shock protein 72; hydrocortisone; interleukin 10; interleukin 6; interleukin 8; lipopolysaccharide; messenger RNA; monocyte chemotactic protein 1; glutamine; heat shock protein 72; lipopolysaccharide; messenger RNA, Article; clinical article; controlled study; critically ill patient; disease severity; heat shock; human; injury; lymphocyte; monocyte; peripheral blood mononuclear cell; protein expression; sepsis; single nucleotide polymorphism; systemic inflammatory response syndrome; cell culture; dose response; drug effects; genetics; heat shock response; immunology; injury; lymphocyte; metabolism; monocyte; pathology; sepsis; systemic inflammatory response syndrome, Cells, Cultured; Dose-Response Relationship, Drug; Glutamine; Heat-Shock Response; HSP72 Heat-Shock Proteins; Humans; Lipopolysaccharides; Lymphocytes; Monocytes; RNA, Messenger; Sepsis; Systemic Inflammatory Response Syndrome; Wounds and Injuries
