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ABSTRACT: Background
Septic shock (SS) is deadly. Sepsis-immune response transitions from an endotoxin-sensitive, hyper-inflammatory phase to an endotoxin-tolerant hypo-inflammatory phase. In mice, we implicated sirtuin 2 (SIRT2) for prolonged hypo-inflammation using leukocyte adhesion, the earliest in vivo inflammatory response to cytokine, chemokine, and metabolite stimuli. The role of SIRT2 in human sepsis remains unknown. We hypothesized that: 1. Peripheral blood mononuclear cells (PBMCs) adhesion response can be used as a physiological biomarker of hypo-inflammation, and 2. SIRT2 regulates the functions of PBMCs and macrophages during the hypo-inflammatory phase of human sepsis.Methods
We stimulated control and SS-whole blood and PBMCs ± lipopolysaccharide (LPS) and investigated
SUBMITTER: Shrestha D
PROVIDER: S-EPMC12823044 | biostudies-literature | 2025 Dec
REPOSITORIES: biostudies-literature