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脑膜炎球菌血症中血浆集落刺激因子浓度的差异变化

Differential alterations in plasma colony-stimulating factor concentrations in meningococcaemia.

作者信息

Waring P M, Presneill J, Maher D W, Layton J E, Cebon J, Waring L J, Metcalf D

机构信息

Cancer Research Unit, Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.

出版信息

Clin Exp Immunol. 1995 Dec;102(3):501-6. doi: 10.1111/j.1365-2249.1995.tb03844.x.

Abstract

To determine whether circulating levels of any of the colony-stimulating factors (CSF) might contribute to the host response in severe sepsis, plasma concentrations of granulocyte CSF (G-CSF), granulocyte-macrophage CSF (GM-CSF), and macrophage CSF (M-CSF) were measured by immunoassays in 20 subjects with meningococcaemia, a bloodstream infection caused by Neisseria meningitidis, that has proven to be a valuable model to study the responses of other inflammatory mediators during sepsis and septic shock in humans. Plasma G-CSF concentrations were transiently elevated in most subjects during the early phase of meningococcaemia, and were higher in subjects with septic shock (mean +/- s.d. = 165 +/- 142 ng/ml, n = 9) compared with those who remained normotensive (mean +/- s.d. = 7 +/- 2 ng/ml, n = 10) (P < 0.05). Peak plasma G-CSF concentrations > 10 ng/ml were associated with the development of septic shock (P < 0.01), disseminated intravascular coagulation (P < 0.01), fulminant infection (P < 0.05), and a fatal outcome (P < 0.01). Plasma GM-CSF concentrations > 1 ng/ml were briefly present in subjects with life-threatening septic shock (1-15 ng/ml, n = 5), and were strongly associated with fulminant meningococcaemia (P < 0.01). Plasma M-CSF concentrations were marginally elevated in all subjects, but were not associated with complications related to or arising from sepsis-induced organ injury. This study demonstrates that plasma levels of G-CSF, GM-CSF and M-CSF show very different responses during meningococcaemia, changes which presumably reflect the different roles played by these mediators in sepsis and, potentially, in septic shock.

摘要

为了确定任何一种集落刺激因子(CSF)的循环水平是否可能在严重脓毒症中对宿主反应有影响,通过免疫测定法测量了20例患脑膜炎球菌血症(一种由脑膜炎奈瑟菌引起的血流感染,已被证明是研究人类脓毒症和脓毒性休克期间其他炎症介质反应的有价值模型)患者的血浆中粒细胞集落刺激因子(G-CSF)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)和巨噬细胞集落刺激因子(M-CSF)的浓度。在脑膜炎球菌血症早期,大多数患者的血浆G-CSF浓度短暂升高,与血压正常者(平均值±标准差=7±2 ng/ml,n=10)相比,脓毒性休克患者(平均值±标准差=165±142 ng/ml,n=9)的血浆G-CSF浓度更高(P<0.05)。血浆G-CSF浓度峰值>10 ng/ml与脓毒性休克的发生(P<0.01)、弥散性血管内凝血(P<0.01)、暴发性感染(P<0.05)和致命结局(P<0.01)相关。血浆GM-CSF浓度>1 ng/ml在有危及生命的脓毒性休克患者中短暂出现(1-15 ng/ml,n=5),并与暴发性脑膜炎球菌血症密切相关(P<0.01)。所有患者的血浆M-CSF浓度略有升高,但与脓毒症诱导的器官损伤相关或由其引起的并发症无关。这项研究表明,在脑膜炎球菌血症期间,血浆G-CSF、GM-CSF和M-CSF水平表现出非常不同的反应,这些变化可能反映了这些介质在脓毒症以及可能在脓毒性休克中所起的不同作用。

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