Briassouli Efrossini, Tzanoudaki Marianna, Goukos Dimitris, Routsi Christina, Nanas Serafim, Vardas Kostas, Apostolou Kleovoulos, Kanariou Maria, Daikos George, Briassoulis George
First Department of Propaedeutic Internal Medicine, University of Athens, Athens, Greece.
Department of Immunology-Histocompatibility, Specialized Center & Referral Center for Primary Immunodeficiencies-Paediatric Immunology, "Aghia Sophia" Children's Hospital, Athens, Greece.
Biomed Res Int. 2015;2015:806042. doi: 10.1155/2015/806042. Epub 2015 Oct 13.
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.
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.
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.
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.
我们评估了严重脓毒症（SS）或创伤相关全身炎症反应综合征（SIRS）患者外周血单核细胞（PBMCs）中脂多糖（LPS）或热休克（HS）对热休克蛋白-72（HSP72）的诱导作用，并与健康个体（H）进行比较；我们还研究了治疗前或治疗后调节谷氨酰胺（Gln）的效果。
将SS组（11例）、SIRS组（10例）和H组（19例）的PBMCs与1μg/mL LPS或43°C热休克进行孵育。在诱导前1小时或诱导后1小时添加10mM Gln，或根本不添加。我们测量了单核细胞（m）、淋巴细胞（l）、mRNA HSP72、HSP72多态性、白细胞介素（ILs）、单核细胞趋化蛋白-1（MCP-1）和皮质醇水平。
与H组相比，SS组的基线lHSP72较高（p < 0.03），SIRS组的mHSP72较高（p < 0.02）。仅热休克诱导l/mHSP72/mRNA HSP72；LPS诱导IL-6、IL-8、IL-10和MCP-1。诱导的mRNA与l/mHSP72相关，且与细胞因子呈负相关。细胞内l/mHSP72/HSP72 mRNA与血清ILs相关，不受皮质醇、疾病严重程度和HSP72多态性的影响。Gln在任何组中均未诱导mRNA，但在LPS/热休克诱导后不可预测地改变了l/mHSP72。
危重症患者中HSP72 mRNA和l/mHSP72较高，热休克可进一步诱导，脂多糖则不能。HSP72蛋白和HSP72 mRNA与血清ILs相关，与上清液细胞因子呈负相关，不受HSP72多态性、皮质醇或疾病严重程度的影响。谷氨酰胺在脂多糖暴露后可能降低l/mHSP72，在热休克诱导后可能增强，但可能不影响早期诱导的HSP72 mRNA。
