旋毛虫活化巨噬细胞的过继转移可以改善小鼠模型中Th1和Th2活化的炎症。,Scientific Reports

当前位置： X-MOL 学术 › Sci. Rep. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

旋毛虫活化巨噬细胞的过继转移可以改善小鼠模型中Th1和Th2活化的炎症。
Scientific Reports ( IF 3.8 ) Pub Date : 2019-04-25 , DOI: 10.1038/s41598-019-43057-1
Shin Ae Kang ₁ , Mi-Kyung Park ₁ , Sang Kyun Park ₁ , Jun Ho Choi ₁ , Da In Lee ₁ , So Myong Song ₁ , Hak Sun Yu ₁

Affiliation

旋毛虫是一种人畜共患线虫，食源性寄生虫和螺旋体的感染导致宿主免疫反应和其他免疫病理的抑制。替代激活的巨噬细胞（M2）以及Treg细胞（蠕虫寄生虫进行免疫调节的靶标）在启动和调节宿主对寄生虫的免疫反应中起关键作用。蠕虫调节宿主免疫反应的确切机制尚未完全了解。为了确定寄生虫诱导的M2巨噬细胞的功能，我们比较了从旋毛虫感染的小鼠中获得的M1和M2巨噬细胞与经螺旋藻排泄/分泌（ES）蛋白处理的巨噬细胞对实验性肠道炎症和过敏性气道的影响炎。T. 螺旋体感染通过增加CD206，ARG1和Fizz2的表达诱导M2巨噬细胞极化。在一次应用中，我们在诱导葡聚糖硫酸钠（DSS）诱导的结肠炎，卵清蛋白（OVA）-敏化之前，将得自螺旋杆菌感染的小鼠的巨噬细胞和经螺旋藻ES蛋白处理的巨噬细胞引入小鼠尾静脉。，以及OVA挑战。通过确定结肠炎症状的严重程度，结肠长度，组织病理学参数以及与Th1相关的炎性细胞因子水平来评估结肠炎的严重程度。与DSS结肠炎组相比，经螺旋线虫感染的小鼠和经螺旋线虫ES蛋白处理的巨噬细胞在处死时表现出明显较低的疾病活动指数（DAI），并且体重和促炎细胞因子水平的降低幅度较小。通过确定炎症症状的严重程度，气道高反应性（AHR），差异细胞计数，组织病理学参数和Th2相关炎症细胞因子的水平来评估过敏性气道炎症的严重程度。在OVA-alum致敏和OVA攻击后，诱发了严重的过敏性气道炎症，这显着增加了Th2相关细胞因子水平，嗜酸性粒细胞浸润和肺中杯状细胞增生。但是，这些严重的过敏症状在螺旋螺旋体感染的小鼠和螺旋螺旋体ES蛋白处理的巨噬细胞中明显减少。蠕虫感染和蠕虫ES蛋白诱导M2巨噬细胞。

"点击查看英文标题和摘要"

Adoptive transfer of Trichinella spiralis-activated macrophages can ameliorate both Th1- and Th2-activated inflammation in murine models.

Trichinella spiralis is a zoonotic nematode and food borne parasite and infection with T. spiralis leads to suppression of the host immune response and other immunopathologies. Alternative activated macrophages (M2) as well as Treg cells, a target for immunomodulation by the helminth parasite, play a critical role in initiating and modulating the host immune response to parasite. The precise mechanism by which helminths modulate host immune response is not fully understood. To determine the functions of parasite-induced M2 macrophages, we compared the effects of M1 and M2 macrophages obtained from Trichinella spiralis-infected mice with those of T. spiralis excretory/secretory (ES) protein-treated macrophages on experimental intestinal inflammation and allergic airway inflammation. T. spiralis infection induced M2 macrophage polarization by increasing the expression of CD206, ARG1, and Fizz2. In a single application, we introduced macrophages obtained from T. spiralis-infected mice and T. spiralis ES protein-treated macrophages into mice tail veins before the induction of dextran sulfate sodium (DSS)-induced colitis, ovalbumin (OVA)-alum sensitization, and OVA challenge. Colitis severity was assessed by determining the severity of colitis symptoms, colon length, histopathologic parameters, and Th1-related inflammatory cytokine levels. Compared with the DSS-colitis group, T. spiralis-infected mice and T. spiralis ES protein-treated macrophages showed significantly lower disease activity index (DAI) at sacrifice and smaller reductions of body weight and proinflammatory cytokine level. The severity of allergic airway inflammation was assessed by determining the severity of symptoms of inflammation, airway hyperresponsiveness (AHR), differential cell counts, histopathologic parameters, and levels of Th2-related inflammatory cytokines. Severe allergic airway inflammation was induced after OVA-alum sensitization and OVA challenge, which significantly increased Th2-related cytokine levels, eosinophil infiltration, and goblet cell hyperplasia in the lung. However, these severe allergic symptoms were significantly decreased in T. spiralis-infected mice and T. spiralis ES protein-treated macrophages. Helminth infection and helminth ES proteins induce M2 macrophages. Adoptive transfer of macrophages obtained from helminth-infected mice and helminth ES protein-activated macrophages is an effective treatment for preventing and treating airway allergy in mice and is promising as a therapeutic for treating inflammatory diseases.

更新日期：2019-04-25

点击分享查看原文

点击收藏

公开下载

阅读更多本刊新发论文本刊介绍/投稿指南