An oligodeoxynucleotide capable of lessening acute lung inflammatory injury in mice infected by influenza virus
An oligodeoxynucleotide capable of lessening acute lung inflammatory injury in mice infected by influenza virus
复制标题
一种寡脱氧核苷酸，能够减轻流感病毒感染小鼠的急性肺部炎症损伤。
DOI：
10.1016/j.bbrc.2011.10.062
复制
发表时间：
2011-11-18
影响因子：
3.1
通讯作者：
Hua, Shucheng
中科院分区：
文献类型：
--
作者：
Fang, Mingli;Wan, Min;Hua, Shucheng
流感病毒感染可导致急性肺炎性损伤(ALI)，这至少部分是由过度的先天免疫反应引起的。为了研究下调Toll样受体(TLR)介导的先天免疫反应是否能减轻流感病毒诱导的Alii，采用体外抑制TLR7/9激活的微卫星DNA SATO5f治疗FM1病毒感染的小鼠。同时，以两个体外活性较低或没有活性的MS ODN MS19和MS33作为对照。出乎意料的是，SATO5f未能减轻小鼠的肺部炎症，而MS19则显著抑制了小鼠的体重减轻，并通过减少小鼠肺部的实变、出血、肺泡内水肿和中性粒细胞浸润而显示出显著的减轻肺部炎症的作用。同时。MS19可降低流感病毒感染小鼠的死亡率，并下调其肺组织中TNE-α的生成。提示MS19可能通过减少TINIF-α的过量产生而发挥其对流感病毒诱导的ALI的治疗作用。(C)2011 Elsevier Inc.保留所有权利。
Infection of influenza virus could induce acute lung inflammatory injury (ALII) that was at least partially caused by excessive innate immune responses. To study whether down-regulating Toll-like receptor (TLR)-mediated innate immune response could lessen influenza virus-induced ALII, a microsatellite DNA mimicking oligodeoxynucleotide (MS ODN), named as SATO5f capable of inhibiting TLR7/9-activation in vitro, was used to treat mice infected with FM1 virus. In parallel, two MS ODNs confirmed with less or no in vitro activities, named as MS19 and MS33, were used as controls. Unexpectedly, SATO5f failed to lessen ALII in the mice, whereas MS19 significantly inhibited the weight loss and displayed dramatic effect on lessening the ALII by reducing consolidation, hemorrhage, intra-alveolar edema and neutrophils infiltration in lungs of the mice. Meanwhile. MS19 could decrease the mortality of influenza virus infected mice and down-regulate TNE-alpha production in their lungs. The data suggest that MS19 might display its therapeutic role on ALII induced by influenza virus by reducing over-production of TINIF-alpha. (C) 2011 Elsevier Inc. All rights reserved.