Traumatic injury, early gene expression, and gram-negative bacteremia.
Traumatic injury, early gene expression, and gram-negative bacteremia.
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DOI：
10.1097/ccm.0000000000000218
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发表时间：
2014-06
影响因子：
8.8
通讯作者：
O'Keefe GE
中科院分区：
文献类型：
--
作者：
Thompson CM;Park CH;Maier RV;O'Keefe GE
菌血症创伤患者的死亡风险高于非菌血症患者。免疫改变在菌血症发生中所起的作用尚不清楚。使用现有的数据集，我们试图确定损伤后早期免疫相关基因表达的差异是否与随后的革兰氏阴性菌血症（GNB）相关。回顾性队列研究，对 Glue Grant 数据库的二次分析。严重钝挫伤患者。美国有七个一级创伤中心。对发生 GNB 的受试者和未发生 GNB 的受试者之间的总白细胞基因表达进行了比较。我们观察到GNB是死亡的独立危险因素（OR，1.86；P=0.015）。然后，我们比较了 10 名随后发展为 GNB 的受试者与 26 名未发展为 GNB 的受试者在受伤后 12 小时和 96 小时时的基因表达。 12小时时，64个探针的表达差异≥1.5倍；没有一个代表与先天性或适应性免疫相关的基因。到96小时，102个探针差异表达，其中20个代表15个先天性或适应性免疫基因；包括 IL1B 的下调和 IL1R2 的上调，反映了 GNB 受试者先天免疫的抑制。我们还观察到 GNB 受试者中适应性免疫基因的下调。损伤后 96 小时，与 GNB 发展相关的白细胞基因表达出现差异，反映了先天免疫和适应性免疫的抑制。创伤后 GNB 部分是宿主免疫失败的结果，标准感染控制技术可能无法完全预防。
Bacteremic trauma victims have a higher risk of death than their non-bacteremic counterparts. The role that altered immunity plays in the development of bacteremia is unknown. Using an existing dataset, we sought to determine if differences in early post-injury immune-related gene expression are associated with subsequent gram-negative bacteremia (GNB). Retrospective cohort study, a secondary analysis of the Glue Grant database. Severely injured blunt trauma patients. Seven level one trauma centers across the United States. Total leukocyte gene expression was compared between the subjects that developed GNB and those that did not. We observed that GNB was an independent risk factor for death (OR, 1.86; P=0.015). We then compared gene expression at 12 and 96 hours after injury in ten subjects who subsequently developed GNB matched to 26 that did not. At 12 hours, expression of 64 probes differed ≥1.5-fold; none represented genes related to innate or adaptive immunity. By 96 hrs, 102 probes were differentially expressed with 20 representing 15 innate or adaptive immunity genes; including downregulation of IL1B and upregulation of IL1R2, reflecting suppression of innate immunity in GNB subjects. We also observed downregulation of adaptive immune genes in the GNB subjects. By 96 hours after injury, there are differences in leukocyte gene expression associated with the development of GNB, reflecting suppression of both innate and adaptive immunity. GNB after trauma is, in part, consequence of host immunity failure and may not be completely preventable by standard infection-control techniques.