这项研究旨在通过评估炎症介质和单核细胞极化标志物的基因表达来鉴定出院后败血症患者的单核细胞改变。有人假设败血症会重新编程单核细胞的炎症状态，导致出院后持续存在的影响并影响患者的预后。
方法：炎症受体的基因表达模式，M1和M2巨噬细胞极化标记，NLRP3炎性体成分，并评估单核细胞中的促炎和抗炎细胞因子。
方法：来自圣保罗大学医院的34名患者，在急性脓毒症阶段（A阶段），ICU出院后立即（B阶段），3个月（C期），6个月（D期），1年（E阶段），出院后3年(F期)，包括在内。在A和B阶段死亡的患者分别分组，其余患者统称为幸存者组.
结果：Toll样受体（TLR）2和TLR4（炎性受体）的基因表达，NLRP3，NFκB1，衔接分子凋亡相关斑点样蛋白，含有CARD，caspase1、caspase11和caspase12（NLRP3炎性体成分），白细胞介素-1α，白细胞介素-1β，白细胞介素18和高迁移率族蛋白1（促炎细胞因子），白介素-10（抗炎细胞因子），C-X-C基序趋化因子配体10，C-X-C基序趋化因子配体11和白介素-12p35（M1炎性极化标记），和C-C基序趋化因子配体14，C-C基序趋化因子配体22，转化生长因子-β（TGF-β），与对照组相比，从A期到E期，单核细胞中的SR-B1和过氧化物酶体增殖物激活受体γ（M2抗炎极化和组织修复标志物）上调。
结论：脓毒症重新编程单核细胞的炎症状态，可能导致脓毒症后综合征的发展和死亡率。
This
study sought to identify monocyte alterations from septic patients after hospital discharge by evaluating gene expression of inflammatory mediators and monocyte polarization markers. It was hypothesized that sepsis reprograms the inflammatory state of monocytes, causing effects that persist after hospital discharge and influencing patient outcomes.
METHODS: The gene expression patterns of inflammatory receptors, M1 and M2 macrophage polarization markers, NLRP3 inflammasome components, and pro- and anti-inflammatory cytokines in monocytes were assessed.
METHODS: Thirty-four patients from the University of São Paulo Hospital, during the acute sepsis phase (phase A), immediately after ICU discharge (phase B), and 3 months (phase C), 6 months (phase D), 1 year (phase E), and 3 years (phase F) after discharge, were included. Patients that died during phases A and B were grouped separately, and the remaining patients were collectively termed the survivor group.
RESULTS: The gene expression of toll-like receptor (TLR)2 and TLR4 (inflammatory receptors), NLRP3, NFκB1, adaptor molecule apoptosis-associated speck-like protein containing a CARD, caspase 1, caspase 11, and caspase 12 (NLRP3 inflammasome components), interleukin-1α, interleukin-1β, interleukin-18, and high-mobility group box 1 protein (proinflammatory cytokines), interleukin-10 (anti-inflammatory cytokine), C-X-C motif chemokine ligand 10, C-X-C motif chemokine ligand 11, and interleukin-12p35 (M1 inflammatory polarization markers), and C-C motif chemokine ligand 14, C-C motif chemokine ligand 22, transforming growth factor-beta (TGF-β), SR-B1, and peroxisome proliferator-activated receptor γ (M2 anti-inflammatory polarization and tissue repair markers) was upregulated in monocytes from phase A until phase E compared with the control group.
CONCLUSIONS: Sepsis reprograms the inflammatory state of monocytes, probably contributing to postsepsis syndrome development and mortality.
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