IL-35 is elevated in clinical and experimental sepsis and mediates inflammation
IL-35 is elevated in clinical and experimental sepsis and mediates inflammation
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IL-35 在临床和实验性脓毒症中升高并介导炎症
DOI：
10.1016/j.clim.2015.08.016
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发表时间：
2015-12-01
影响因子：
8.6
通讯作者：
Zhang, Liping
中科院分区：
文献类型：
--
作者：
Cao, Ju;Xu, Fang;Zhang, Liping
败血症的发病率和死亡率相当高。IL-35是一种新近发现的细胞因子，在感染和免疫中起调节作用。在这项研究中，我们发现，IL-35浓度在成人或儿童脓毒症患者的血清样品中显着高于从健康对照组。IL-35随着脓毒症严重程度的增加而逐渐升高。血清IL-35升高与LOD（逻辑器官功能障碍）或SAPS II（简化急性生理学评分）评分相关，并与炎症标志物相关。在小鼠腹腔脓毒症中，抗IL-35 p35抗体的施用显著减少了脓毒症动物中细菌的传播，这伴随着增强的局部中性粒细胞募集和早期增加的炎性细胞因子和趋化因子的释放。因此，脓毒症与IL-35的释放增强相关。在腹腔脓毒症中，IL-35可能促进细菌传播。IL-35在脓毒症的免疫发病机制中起主要作用。(C)2015 Elsevier Inc. All rights reserved.
Sepsis carries considerable morbidity and mortality. IL-35 is a newly described cytokine, which plays a regulatory role in infection and immunity. In this study, we found that IL-35 concentration in serum samples from adult or child patients with sepsis was significantly higher compared with that from healthy controls. IL-35 gradually increased according to sepsis severity. Increased serum IL-35 was associated with LOD (Logistic Organ Dysfunction) or SAPS II (Simplified Acute Physiology Score) scores, and correlated with markers of inflammation. In murine abdominal sepsis, administration of anti-IL-35 p35 antibodies significantly diminished dissemination of the bacteria in septic animals, which was accompanied by enhanced local neutrophil recruitment and early increased release of inflammatory cytokines and chemokines. Therefore, sepsis is associated with enhanced release of IL-35. In abdominal sepsis, IL-35 likely facilitates bacterial dissemination. IL-35 plays a major role in the immunopathogenesis of sepsis. (C) 2015 Elsevier Inc. All rights reserved.