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旋毛虫感染通过募集CD4(+)CD25(+)Foxp3(+) T细胞抑制肠道炎症。

Trichinella spiralis infection suppressed gut inflammation with CD4(+)CD25(+)Foxp3(+) T cell recruitment.

作者信息

Cho Min Kyoung, Park Mi Kyung, Kang Shin Ae, Choi Seon Hee, Ahn Soon Cheol, Yu Hak Sun

机构信息

Department of Parasitology, Pusan National University School of Medicine, Busan 626-813, Korea.

出版信息

Korean J Parasitol. 2012 Dec;50(4):385-90. doi: 10.3347/kjp.2012.50.4.385. Epub 2012 Nov 26.

Abstract

In order to know the effect of pre-existing Trichinella spiralis infection on experimentally induced intestinal inflammation and immune responses, we induced colitis in T. spiralis-infected mice and observed the severity of colitis and the levels of Th1, Th2, and regulatory cytokines and recruitment of CD4(+)CD25(+)Foxp3(+) T (regulatory T; T(reg)) cells. Female C57BL/6 mice were infected with 250 muscle larvae; after 4 weeks, induction of experimental colitis was performed using 3% dextran sulfate sodium (DSS). During the induction period, we observed severity of colitis, including weight loss and status of stool, and evaluated the disease activity index (DAI). A significantly low DAI and degree of weight loss were observed in infected mice, compared with uninfected mice. In addition, colon length in infected mice was not contracted, compared with uninfected mice. We also observed a significant increase in production of pro-inflammatory cytokines, IL-6 and IFN-γ, in spleen lymphocytes treated with DSS; however, such an increase was not observed in infected mice treated with DSS. Of particular interest, production of regulatory cytokines, IL-10 and transforming growth factor (TGF)-β, in spleen lymphocytes showed a significant increase in mice infected with T. spiralis. A similar result was observed in mesenteric lymph nodes (MLN). Subsets of the population of T(reg) cells in MLN and spleen showed significant increases in mice infected with T. spiralis. In conclusion, T. spiralis infection can inhibit the DSS-induced colitis in mice by enhancing the regulatory cytokine and T(reg) cells recruitment.

摘要

为了解预先存在的旋毛虫感染对实验性诱导的肠道炎症和免疫反应的影响,我们在感染旋毛虫的小鼠中诱导结肠炎,并观察结肠炎的严重程度、Th1、Th2和调节性细胞因子水平以及CD4(+)CD25(+)Foxp3(+)T(调节性T细胞;T(reg)细胞)的募集情况。雌性C57BL/6小鼠感染250条肌幼虫;4周后,使用3%葡聚糖硫酸钠(DSS)诱导实验性结肠炎。在诱导期,我们观察结肠炎的严重程度,包括体重减轻和粪便状况,并评估疾病活动指数(DAI)。与未感染小鼠相比,感染小鼠的DAI显著降低,体重减轻程度也较低。此外,与未感染小鼠相比,感染小鼠的结肠长度未收缩。我们还观察到,用DSS处理的脾淋巴细胞中促炎细胞因子IL-6和IFN-γ的产生显著增加;然而,在用DSS处理的感染小鼠中未观察到这种增加。特别值得注意的是,感染旋毛虫的小鼠脾淋巴细胞中调节性细胞因子IL-10和转化生长因子(TGF)-β的产生显著增加。在肠系膜淋巴结(MLN)中也观察到了类似的结果。感染旋毛虫的小鼠MLN和脾中T(reg)细胞群体的亚群显著增加。总之,旋毛虫感染可通过增强调节性细胞因子和T(reg)细胞募集来抑制DSS诱导的小鼠结肠炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcab/3514436/e82aa1f88ecc/kjp-50-385-g001.jpg

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