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Chemokine C10 Promotes Disease Resolution and Survival in an Experimental Model of Bacterial Sepsis

机译：趋化因子C10在细菌性脓毒症的实验模型中促进疾病的解决和生存

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Previous studies have suggested that the C-C chemokine C10 is involved in the chronic stages of host defense reactions. The present study addressed the role of C10 in a murine model of septic peritonitis, induced by cecal ligation and puncture (CLP). Unlike other C-C chemokines, C10 levels in the peritoneal wash were increased approximately 30-fold above baseline levels at 48 h after CLP surgery. Immunoneutralization of peritoneal C10 levels with polyclonal anti-C10 antiserum during CLP-induced peritonitis negatively impacted mouse survival over 4 days. In contrast, when 500 ng of recombinant murine C10 was administered immediately after CLP surgery, the 4-day survival rate increased from 20% to over 60%. The C10 therapy appeared to facilitate a rapid and significant enhancement of the levels of tumor necrosis factor alpha (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) and a later increase in interleukin-13 (IL-13) levels in the peritoneal cavity. In vitro studies showed that the combination of IL-1β and C10 markedly augmented TNF-α synthesis by peritoneal macrophages and that C10 synthesis was induced in these cells following their exposure to IL-13. At 24 h after CLP surgery, only 25% of C10-treated mice were bacteremic versus 85% of the control group that exhibited dissemination of bacteria into the circulation. The lack of bacteremia in C10-treated mice appeared to be related, in part, to in vitro evidence that C10 significantly enhanced the bacterial phagocytic activity of peritoneal macrophages. In addition, in vivo evidence suggested that C10 therapy significantly reduced the amount of material that leaked from the damaged gut. Taken together, the results of this study demonstrate that the C10 chemokine rapidly promotes disease resolution in the CLP model through its direct effects on the cellular events critically involved in host defense during septic peritonitis.
机译：先前的研究表明C-C趋化因子C10参与宿主防御反应的慢性阶段。本研究探讨了C10在盲肠结扎和穿刺（CLP）诱导的败血症性腹膜炎小鼠模型中的作用。与其他C-C趋化因子不同，CLP手术后48小时，腹膜冲洗液中的C10水平比基线水平增加了约30倍。在CLP诱发的腹膜炎期间，用多克隆抗C10抗血清对腹膜C10水平进行免疫原化治疗会对小鼠存活超过4天产生负面影响。相反，在CLP手术后立即给予500 ng重组鼠C10，则4天生存率从20％增加到60％以上。 C10疗法似乎促进了肿瘤坏死因子α（TNF-α）和单核细胞趋化蛋白1（MCP-1）的水平的快速和显着增强，以及随后白细胞介素13（IL-13）水平的升高。腹腔。体外研究表明，IL-1β和C10的组合通过腹膜巨噬细胞显着增强了TNF-α的合成，并且在这些细胞暴露于IL-13后诱导了C10的合成。在进行CLP手术后24小时，只有25％的C10处理小鼠具有细菌性，而对照组的85％则表现出细菌向循环中传播。在用C10处理的小鼠中缺乏菌血症似乎部分与体外证据有关，即C10显着增强了腹膜巨噬细胞的细菌吞噬活性。此外，体内证据表明，C10治疗可显着减少从受损肠道泄漏的物质量。两者合计，这项研究的结果表明，C10趋化因子通过其对败血症性腹膜炎期间与宿主防御至关重要的细胞事件直接相关的直接作用，快速促进CLP模型中的疾病消退。

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