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旋毛虫重组 53kDa 蛋白对实验性结肠炎小鼠的保护作用。

The protective effect of the recombinant 53-kDa protein of Trichinella spiralis on experimental colitis in mice.

机构信息

Department of General Internal Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.

出版信息

Dig Dis Sci. 2011 Oct;56(10):2810-7. doi: 10.1007/s10620-011-1689-8. Epub 2011 Apr 8.

Abstract

BACKGROUND

Helminth infection has been proven to reduce the severity of experimental inflammatory bowel disease (IBD). The excretory-secretory proteins of helminths play an important role in the process of immunomodulation.

AIMS

In the present study, we aimed to investigate the protective potential of recombinant Trichinella spiralis (TS) 53-kDa protein (rTsP53), a component of excretory-secretory proteins, on experimental colitis in mice.

METHODS

BALB/c mice were treated subcutaneously with 50 μg rTsP53 three times at an interval of 5 days. Colitis was induced by intrarectal administration of 5 mg trinitrobenzene sulfonic acid (TNBS). Disease activities and macroscopic and microscopic scores were evaluated. To determine immune response provoked by rTsP53, we measured specific IgG1 and IgG2a values against rTsP53 in sera of mice. We also detected cytokine profiles as well as the markers of alternatively activated macrophages (M2) in mice.

RESULTS

RTsP53 ameliorated significantly the disease activity index (DAI) as well as the macroscopic and microscopic scores. IgG1 but not IgG2a was the predominant specific antibody detected in the sera of immunized mice, indicating the potential of stimulating T-helper (Th) 2 bias response by rTsP3. Pre-treatment with rTsP53 decreased serum Th1 cytokines (TNF-a, IFN-γ) and elevated serum levels of serum Th2 cytokines (IL-4, IL-13); it also decreased colonic Th1 cytokines (TNF-α, IL-6) and colonic regulatory cytokines (IL-10, TGF-β1). RTsP53 increased colonic M2 markers, arginase-1 (Arg-1), and found in inflammatory zone 1 (FIZZ1), compared to mice without rTsP53 pretreatment.

CONCLUSIONS

RTsP53 is a potential protective agent for IBD.

摘要

背景

寄生虫感染已被证实可减轻实验性炎症性肠病(IBD)的严重程度。寄生虫的排泄-分泌蛋白在免疫调节过程中发挥重要作用。

目的

本研究旨在探讨重组旋毛虫(TS)53kDa 蛋白(rTsP53)作为排泄-分泌蛋白的一个组成部分对实验性结肠炎小鼠的保护潜力。

方法

BALB/c 小鼠经皮皮下注射 50μg rTsP53,每隔 5 天 3 次。通过直肠内给予 5mg 三硝基苯磺酸(TNBS)诱导结肠炎。评估疾病活动度和宏观及微观评分。为了确定 rTsP53 引起的免疫反应,我们测量了血清中针对 rTsP53 的特异性 IgG1 和 IgG2a 值。我们还检测了细胞因子谱以及小鼠中替代激活的巨噬细胞(M2)的标志物。

结果

rTsP53 显著改善了疾病活动指数(DAI)以及宏观和微观评分。免疫小鼠血清中检测到的主要特异性抗体是 IgG1,而不是 IgG2a,表明 rTsP3 具有刺激 T 辅助(Th)2 偏倚反应的潜力。rTsP53 预处理降低了血清 Th1 细胞因子(TNF-a、IFN-γ)水平,升高了血清 Th2 细胞因子(IL-4、IL-13)水平;它还降低了结肠 Th1 细胞因子(TNF-α、IL-6)和结肠调节细胞因子(IL-10、TGF-β1)。与未用 rTsP53 预处理的小鼠相比,rTsP53 增加了结肠 M2 标志物精氨酸酶-1(Arg-1)和炎症区域 1(FIZZ1)的表达。

结论

rTsP53 是 IBD 的一种潜在保护剂。

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