Tsuda Yasuhiro, Kobayashi Makiko, Herndon David N, Suzuki Fujio
Department of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, USA.
Burns. 2008 Jun;34(4):460-6. doi: 10.1016/j.burns.2007.07.004. Epub 2007 Oct 29.
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.
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。