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通过增加小鼠黏膜Th2细胞减轻三硝基苯磺酸诱导的结肠炎。

attenuates TNBS-induced colitis via increasing mucosal Th2 cells in mice.

作者信息

Wu Yi-Zhong, Tan Gao, Wu Fang, Zhi Fa-Chao

机构信息

Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Department of Gastroenterology, Hunan Provincial People's Hospital, Changsha, China.

出版信息

Oncotarget. 2017 May 18;8(43):73810-73816. doi: 10.18632/oncotarget.17962. eCollection 2017 Sep 26.

DOI:10.18632/oncotarget.17962
PMID:29088747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5650302/
Abstract

There is an epidemiological inverse relationship between () infection and Crohn's disease (CD). However, whether plays a protective role against CD remains unclear. Since 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis is thought to resemble CD, we investigated whether can attenuate TNBS-induced colitis in mice. Here we show that can attenuate the severity of TNBS-induced colitis. In addition, not only down-regulates Th17 and Th1 cytokine expression, but can up-regulate Th2 cytokine expression and increase the Th2:Th17 ratio of CD4 T in the colonic mucosa of TNBS-induced colitis. Our results indicate that attenuates TNBS-induced colitis mainly through increasing Th2 cells in murine colonic mucosa. Our finding offers a novel view on the role of in regulating gastrointestinal immunity, and may open a new avenue for development of therapeutic strategies in CD by making use of asymptomatic colonization.

摘要

()感染与克罗恩病(CD)之间存在流行病学上的负相关关系。然而,其是否对CD起保护作用仍不清楚。由于2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎被认为类似于CD,我们研究了其是否能减轻小鼠TNBS诱导的结肠炎。在此我们表明其能减轻TNBS诱导的结肠炎的严重程度。此外,其不仅下调Th17和Th1细胞因子表达,还能上调Th2细胞因子表达,并增加TNBS诱导的结肠炎小鼠结肠黏膜中CD4 T细胞的Th2:Th17比例。我们的结果表明其主要通过增加小鼠结肠黏膜中的Th2细胞来减轻TNBS诱导的结肠炎。我们的发现为其在调节胃肠道免疫中的作用提供了新观点,并可能通过利用无症状的()定植为CD治疗策略的开发开辟新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/93d27d85ca5a/oncotarget-08-73810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/ceed4e6346a3/oncotarget-08-73810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/5b3bedc3d518/oncotarget-08-73810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/040a03b0bd79/oncotarget-08-73810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/93d27d85ca5a/oncotarget-08-73810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/ceed4e6346a3/oncotarget-08-73810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/5b3bedc3d518/oncotarget-08-73810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/040a03b0bd79/oncotarget-08-73810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81b3/5650302/93d27d85ca5a/oncotarget-08-73810-g004.jpg

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