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在人类脓毒症中,趋化因子单核细胞趋化蛋白-1和-2的血浆水平升高。

Plasma levels of the chemokines monocyte chemotactic proteins-1 and -2 are elevated in human sepsis.

作者信息

Bossink A W, Paemen L, Jansen P M, Hack C E, Thijs L G, Van Damme J

机构信息

Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands.

出版信息

Blood. 1995 Nov 15;86(10):3841-7.

PMID:7579352
Abstract

Because of their effects on monocytes, monocyte chemotactic proteins-1 and -2 (MCP-1 and MCP-2) may participate in the pathophysiology of sepsis. We measured circulating MCP-1 and MCP-2 levels in 42 septic patients having positive local or blood cultures. MCP-1 and MCP-2 levels were elevated in 24 (57%) and 25 (59%) of 42 septic patients, respectively, compared with healthy volunteers. Both patients with gram-positive and gram-negative infections had elevated MCP-1 plasma levels (P = .0001) and P < .0001), respectively; Mann-Whitney-U test), whereas patients with gram-positive infection, but not those with gram-negative infection, had increased MCP-2 plasma levels (P= .0182). No relative differences in MCP-1 and MCP-2 plasma levels were observed between several subgroups of patients (sepsis v septic shock; survivors v nonsurvivors), although levels of MCP-1 were the highest in patients with the more severe forms of sepsis, ie, those with shock or a lethal outcome. Serial observations showed that MCP-1 and MCP-2 plasma levels remained elevated for at least 48 hours. MCP-1 correlated weakly with interleukin-8 and MCP-2, the correlations for which were most pronounced in patients with septic shock. MCP-2 correlated with interleukin-8, and surprisingly, with the complement activation product C3a; these correlations further improved when analyzing patients with septic shock or when applying gram-positive infections. Thus, our results not only show increased MCP-1 and MCP-2 levels in patients with sepsis, but also suggest that the synthesis and release of MCP-1 and MCP-2 in sepsis are differently regulated in part.

摘要

由于单核细胞趋化蛋白-1和-2(MCP-1和MCP-2)对单核细胞有影响,它们可能参与脓毒症的病理生理过程。我们检测了42例局部或血培养呈阳性的脓毒症患者循环中的MCP-1和MCP-2水平。与健康志愿者相比,42例脓毒症患者中分别有24例(57%)和25例(59%)的MCP-1和MCP-2水平升高。革兰氏阳性菌感染和革兰氏阴性菌感染的患者MCP-1血浆水平均升高(分别为P = .0001和P < .0001;曼-惠特尼U检验),而革兰氏阳性菌感染的患者MCP-2血浆水平升高(P = .0182),革兰氏阴性菌感染的患者则不然。在几个患者亚组(脓毒症与脓毒性休克;存活者与非存活者)之间未观察到MCP-1和MCP-2血浆水平的相对差异,尽管在脓毒症更严重形式的患者中,即休克或致死结局的患者中MCP-1水平最高。连续观察表明,MCP-1和MCP-2血浆水平至少持续升高48小时。MCP-1与白细胞介素-8和MCP-2的相关性较弱,其中在脓毒性休克患者中相关性最为明显。MCP-2与白细胞介素-8相关,令人惊讶的是,还与补体激活产物C3a相关;在分析脓毒性休克患者或应用革兰氏阳性菌感染时,这些相关性进一步增强。因此,我们的结果不仅显示脓毒症患者的MCP-1和MCP-2水平升高,还表明脓毒症中MCP-1和MCP-2的合成和释放部分受到不同的调节。

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