Glutamine suppresses Hsp72 not Hsp90α and is not inducing Th1, Th2, or Th17 cytokine responses in human septic PBMCs

Effects of prophylactic administration of glutamine on CD4+T cell polarisation and kidney injury in mice with polymicrobial sepsis

“…These findings suggest that a more balanced T cell polarisation was found at late phase of sepsis when pretreated with GLN. An experiment with human PBMC from septic patients revealed that a high dose of GLN could not alter the Th1:Th2 (18) . Since the study mentioned earlier is an ex vivo experiment, the study design may not reflect the actual physiological situation in the body.…”

“…We applied Trizol reagent (Invitrogen) to extract total RNA from renal tissues and CD4 + T cells isolated from spleen. RNA (2•5 μg) was reverse transcribed using a RevertAid First Strand cDNA Synthesis Kit (Thermo Scientific) with oligo (dT) 18 primers, according to standard protocols. A real-time PCR was carried out in optical ninety-six-well plates on an ABI 7300 Real-Time PCR System (Applied Biosystems).…”

“…Parenteral GLN administration after sepsis induction was found to reduce the percentage of IL-17-expressing CD4 + T cells and attenuated the dysregulated immune response in sepsis (17) . However, an ex vivo study showed that high-dose GLN did not induce Th1/Th2/Th17 cytokine responses in peripheral blood mononuclear cells (PBMC) obtained from patients with severe sepsis (18) . Also, GLN administration may repress heat shock protein 72 (HSP72) expression of PBMC after lipopolysaccharide exposure and enhance HSP72 proteins after heat shock induction in patients with sepsis (19) .…”

Alarming levels of heat shock proteins 72 and 90α in critically ill children

“…Little is known about the alarming roles of extracellular HSP72 and HSP90α in the acute phase [1] of sepsis (S) or severe sepsis (SS). We determined serum HSP90α, HSP72 and neutrophil CD64 expression, IL-6, IL-8, IL-10, and TNFα in children with S or SS compared with SIRS (brain injury) or healthy children (H).…”

Polymyxin B hemoperfusion in septic shock: nothing overmuch (Meden Agan)!

“…Last decades the concept of targeted interventions to decrease the circulating mediators of sepsis to intercept the dysregulated host response grew enthusiasm, and endotoxin was a reliable target to consider for therapy. Treatment interventions at various steps of the endotoxin pathway, including the heat shock protein-72 and -90 "danger signal" induction (3), have been tested experimentally in human in vivo and in vitro studies (4,5) without convincing results (6,7). Attempts to remove endotoxin with monoclonal antibodies failed, so extracorporeal removal by hemoperfusion was introduced using polymyxin B cartridges, where endotoxin can be bound and neutralized (8).…”