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去甲肾上腺素激活的中性粒细胞对宿主抗菌抵抗力的损害。

Impairment of the host's antibacterial resistance by norepinephrine activated neutrophils.

作者信息

Tsuda Yasuhiro, Kobayashi Makiko, Herndon David N, Suzuki Fujio

机构信息

Department of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, USA.

出版信息

Burns. 2008 Jun;34(4):460-6. doi: 10.1016/j.burns.2007.07.004. Epub 2007 Oct 29.

Abstract

The susceptibility of mice to infectious complications is dramatically increased in an accompaniment with systemic inflammatory response syndrome (SIRS). Polymorphonuclear neutrophils with immunosuppressive ability (PMN-II) that appear in response to SIRS have been classified as one of the cells responsible for the increased susceptibility of mice with SIRS (SIRS mice) to sepsis induced by cecal-ligation and puncture (CLP). Since a high level of norepinephrine (NE) is demonstrated in the plasma of SIRS mice, in the present study, the role of NE on the appearance of PMN-II in SIRS mice was studied. Similar to SIRS mice, normal mice became susceptible to CLP-induced infectious complications after inoculation with NE-treated PMN. CCL2 and IL-10 (biomarkers for PMN-II) were equally produced by PMN-II prepared from SIRS mice and NE-treated PMN. However, CCL3 and IL-12 (biomarkers for immunostimulatory PMN, PMN-I) were not detected in culture fluids from either PMN preparation. These results indicate that NE mass-produced in association with SIRS development plays a role on the generation of PMN-II and the appearing PMN-II are responsible, in part, for increased susceptibility of SIRS mice to CLP-induced infectious complications.

摘要

伴随着全身炎症反应综合征(SIRS),小鼠对感染性并发症的易感性显著增加。因SIRS而出现的具有免疫抑制能力的多形核中性粒细胞(PMN-II)已被归类为导致SIRS小鼠(SIRS小鼠)对盲肠结扎穿刺(CLP)诱导的脓毒症易感性增加的细胞之一。由于在SIRS小鼠的血浆中显示出高水平的去甲肾上腺素(NE),在本研究中,研究了NE对SIRS小鼠中PMN-II出现的作用。与SIRS小鼠相似,正常小鼠在接种经NE处理的PMN后对CLP诱导的感染性并发症变得易感。CCL2和IL-10(PMN-II的生物标志物)由从SIRS小鼠制备的PMN-II和经NE处理的PMN等量产生。然而,在两种PMN制剂的培养液中均未检测到CCL3和IL-12(免疫刺激性PMN,PMN-I的生物标志物)。这些结果表明,与SIRS发展相关大量产生的NE对PMN-II的产生起作用,并且出现的PMN-II部分地导致SIRS小鼠对CLP诱导的感染性并发症的易感性增加。

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