Song Qianying, Zhou Changming, Liu Yufei, Wang Liping, Lv Huiyi, Zhang Cuiying, Wang Xuanqi
Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Sci Rep. 2025 Jul 1;15(1):21527. doi: 10.1038/s41598-025-07339-1.
Sepsis, one of the leading causes of death in critically ill patients, is characterized by multiple organ dysfunction due to a dysregulated immune response to infection. Caregivers closely monitor patients' organ function indicators in the intensive care unit,which is essential for the early identification and management of organ dysfunction cauxsd by sepsis. Hence, we investigated the effects of CSN6 on sepsis and its underlying mechanism. RAW264.7 cell inducted with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). CSN6 protein expression increased in an in vitro model of sepsis. We collected samples from 10 sepsis patients (It was collected under strict compliance with ethical norms and nursing procedures) and performed single-cell analysis for CSN6 expression. CSN6 aggravated macrophage inflammation in an in vitro model of sepsis. CSN6 aggravated macrophage ferroptosis in an in vitro model of sepsis. CSN6 aggravates mitochondrial damage in an in vitro model of sepsis. CSN6 induces MIF expression in macrophages in an in vitro model of sepsis. MIF inhibitors reduced the effects of CSN6 on inflammation and ferroptosis in an in vitro sepsis model. CSN6 protein at 11-ARG, 21-ARG, 31-LEU, and 32-ASP linked to MIF protein at 280-ASN and 366-SER. In conclusion, CSN6 appears to aggravate inflammation in macrophages in a sepsis model via MIF signaling. This finding suggests that future therapeutic strategier targeting the CSN6 and MIF pathways may require nurses to closely monitor changes in inflammatory responses and potential treatment side effecta at the bedside. Further research involving in vivo models, such as examining CSN6 and MIF expression levels in macrophages or monocytes from sepsis and control mice, is essential to fully confirm these findings and establish the therapeutic potential of targeting the CSN6/MIF axis in sepsis. The nursing research team plays a key role in translating basic research findings into clinical practice,including the developpment of early warning tools and individualized management programs based on these biomarkers.
脓毒症是重症患者主要的死亡原因之一，其特征是由于对感染的免疫反应失调导致多器官功能障碍。在重症监护病房，护理人员密切监测患者的器官功能指标，这对于早期识别和处理由脓毒症引起的器官功能障碍至关重要。因此，我们研究了CSN6对脓毒症的影响及其潜在机制。用脂多糖（LPS）和三磷酸腺苷（ATP）诱导RAW264.7细胞。在脓毒症体外模型中，CSN6蛋白表达增加。我们从10例脓毒症患者中采集样本（样本采集严格遵循伦理规范和护理程序），并对CSN6表达进行单细胞分析。在脓毒症体外模型中，CSN6加剧巨噬细胞炎症。在脓毒症体外模型中，CSN6加剧巨噬细胞铁死亡。在脓毒症体外模型中，CSN6加重线粒体损伤。在脓毒症体外模型中，CSN6诱导巨噬细胞中巨噬细胞迁移抑制因子（MIF）表达。MIF抑制剂可降低CSN6在体外脓毒症模型中对炎症和铁死亡的影响。CSN6蛋白的11-精氨酸、21-精氨酸、31-亮氨酸和32-天冬氨酸与MIF蛋白的280-天冬酰胺和366-丝氨酸相连。总之，在脓毒症模型中，CSN6似乎通过MIF信号通路加剧巨噬细胞炎症。这一发现表明，未来针对CSN6和MIF通路的治疗策略可能需要护士在床边密切监测炎症反应的变化以及潜在的治疗副作用。涉及体内模型的进一步研究，如检测脓毒症小鼠和对照小鼠巨噬细胞或单核细胞中CSN6和MIF的表达水平，对于充分证实这些发现并确定靶向CSN6/MIF轴在脓毒症中的治疗潜力至关重要。护理研究团队在将基础研究成果转化为临床实践中发挥着关键作用，包括基于这些生物标志物开发预警工具和个体化管理方案。
