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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Cytokine patterns in critically ill patients undergoing percutaneous tracheostomy
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Cytokine patterns in critically ill patients undergoing percutaneous tracheostomy

机译:在经皮气管造口术后的危重病患者中的细胞因子模式

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Summary The inflammatory response to acute injury among humans has proved difficult to study due to the significant heterogeneity encountered in actual patients. We set out to characterize the immune response to a model injury with reduced heterogeneity, a tracheostomy, among stable critical care patients, using a broad cytokine panel and clinical data. Twenty‐three critical care patients undergoing percutaneous bedside tracheostomies were recruited in a medical intensive care unit. Blood samples were collected at five intervals during 24‐h peri‐procedure. Patients were followed‐up for 28 days for clinical outcomes. There were no statistically significant changes in any of the cytokines between the five time‐points when studied as a whole cohort. Longitudinal analysis of the cytokine patterns at the individual patient level with a clustering algorithm showed that, notwithstanding the significant heterogeneity observed, the patients’ cytokine responses can be classified into three broad patterns that show increasing, decreasing or no major changes from the baseline. This analytical approach also showed statistically significant associations between cytokines, with those most likely to be associated being interleukin (IL)‐6, granulocyte colony‐stimulating factor (GCSF) and ferritin, as well as a strong tri‐way correlation between GCSF, monocyte chemoattractant protein 1 (MCP1) and macrophage inflammatory protein‐1β (MIP1β). In conclusion, in this standard human model of soft tissue injury, by applying longitudinal analysis at the individual level, we have been able to identify the cytokine patterns underlying the seemingly random, heterogeneous patient responses. We have also identified consistent cytokine interactions suggesting that IL‐6, GCSF, MCP1 and MIP1β are the cytokines most probably driving the immune response to this injury.
机译:发明内容由于实际患者中遇到的显着异质性,难以研究的人类对急性损伤的炎症反应。我们首先使用广泛的细胞因子面板和临床资料来表征对异质性降低的模型损伤的免疫反应,其稳定的关键护理患者中的气管造口术。在医疗密集护理单位中招募了经皮床侧气管术后的二十三名关键护理患者。在24-H peri-provide期间以五个间隔收集血样。患者随访28天进行临床结果。当作为整个队列进行研究时,五个时间点之间的任何细胞因子没有统计学上显着的变化。通过聚类算法对各个患者水平的细胞因子图案的纵向分析表明,尽管观察到的显着异质性,但患者的细胞因子反应可以分为三种广泛的模式,表现出增加,减少或没有基线的重大变化。这种分析方法还显示出细胞因子之间的统计学上显着的关联,最可能与白细胞介素(IL)-6,粒细胞菌落刺激因子(GCSF)和铁蛋白相关的那些,以及GCSF,单核细胞之间的强烈三相相关性化学抑制剂蛋白1(MCP1)和巨噬细胞炎症蛋白-1β(MIP1β)。总之,在该标准的软组织损伤模型中,通过在个体层面上施加纵向分析,我们能够鉴定看似随机,异质患者反应的细胞因子模式。我们还鉴定了一致的细胞因子相互作用,表明IL-6,GCSF,MCP1和MIP1β是最可能推动对这种损伤的免疫应答的细胞因子。

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