IL-33 alleviates DSS-induced chronic colitis in C57BL/6 mice colon lamina propria by suppressing Th17 cell response as well as Th1 cell response.
IL-33 alleviates DSS-induced chronic colitis in C57BL/6 mice colon lamina propria by suppressing Th17 cell response as well as Th1 cell response.
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IL-33 通过抑制 Th17 细胞反应以及 Th1 细胞反应，减轻 C57BL/6 小鼠结肠固有层中 DSS 诱导的慢性结肠炎。
DOI：
10.1016/j.intimp.2015.08.032
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发表时间：
2015-12
影响因子：
5.6
通讯作者：
Sun Xun
中科院分区：
文献类型：
--
作者：
Zhu Junfeng;Wang Yuanyuan;Yang Fangli;Sang Lixuan;Zhai Jingbo;Li Shengjun;Li Yan;Wang Danan;Lu Changlong;Sun Xun
白细胞介素(IL)-33是IL-1细胞因子家族的一员，与包括炎症性肠病（IBD）在内的自身免疫性疾病有关。少数动物模型研究表明，IL-33可以抑制肠系膜淋巴结（MLN）和血清中Th1细胞的反应，提高Th2细胞的反应。然而，关于IL-33对结肠固有层Th17细胞和Th1/Th2细胞的影响，文献报道甚少。本研究旨在探讨IL-33对葡聚糖硫酸钠（DSS）诱导的慢性结肠炎小鼠结肠固有层Th17细胞的影响。我们研究IL-33对结肠炎结肠组织损伤及临床症状的影响。采用流式细胞术检测T细胞亚群，酶联免疫吸附试验（ELISA）和实时荧光定量PCR检测固有层淋巴细胞（LPL）分泌细胞因子的产生。我们发现，rIL-33治疗导致DSS诱导的慢性结肠炎的显著缓解，证据如下：1)体重减轻、DAI、宏观变化和组织学评分；2)下调LPL中Th17和Th1细胞的表达率和绝对细胞数；3)诱导分泌较低水平的IFN-γ和IL-17A。因此，IL-33可能通过抑制Th17反应并将Th1反应转换为Th2反应，在dss诱导的小鼠慢性结肠炎中发挥治疗作用。
Interleukin (IL)-33, a member of the IL-1 cytokine family, is associated with autoimmune diseases including inflammatory bowel diseases (IBD). A few studies on animal models have shown that IL-33 can suppress Th1 cell response and improve Th2 cell response in mesenteric lymph nodes (MLN) and sera. However, there is little data published about the effect of IL-33 on Th17 cell in and Th1/Th2 cell in colon lamina propria. The aim of this study was to investigate the effect of IL-33 on Th17 cell in colon lamina propria of mice with dextran sulfate sodium (DSS) induced chronic colitis. We studied the influence of IL-33 on colonic tissue injury and clinical symptoms of colitis. The T cell subsets were measured by flow cytometry and the production of cytokines secreted by lamina propria lymphocytes (LPL) was measured by Enzyme-Linked Immunosorbent Assay (ELISA) and quantitative real-time PCR. We have found that rIL-33 treatment led to a significant alleviation of DSS induced chronic colitis as evidenced by 1) alleviation of weight loss, DAI, macroscopic changes and histological score; 2) down-regulating the rates and absolute cell numbers of Th17 and Th1 cell in LPL; 3) inducing secretion of lower levels of IFN-γ and IL-17A. It is therefore concluded that IL-33 may play a therapeutic role in DSS-induced chronic colitis in mice by suppressing Th17 response and switching Th1 to Th2 response.
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影响因子：
64.5
作者：
Ivanov, Ivaylo I.;McKenzie, Brent S.;Littman, Dan R.
通讯作者：
Littman, Dan R.
影响因子：
29.7
作者：
Zhu J;Yamane H;Paul WE
通讯作者：
Paul WE
口服给予肠道菌苗超免疫的奶牛的牛奶会刺激小鼠固有层 T 淋巴细胞产生 Th1 偏向的细胞因子。
影响因子：
5.6
作者：
Wang Y;Lin L;Yin C;Othtani S;Aoyama K;Lu C;Sun X;Yoshikai Y
通讯作者：
Yoshikai Y
影响因子：
4.6
作者：
F. Obermeier;G. Kojouharoff;W. Hans;J. Schölmerich;V. Gross;W. Falk
通讯作者：
F. Obermeier;G. Kojouharoff;W. Hans;J. Schölmerich;V. Gross;W. Falk
影响因子：
6.4
作者：
G. Vahedi;Y. Kanno;V. Sartorelli;J. O’Shea
通讯作者：
G. Vahedi;Y. Kanno;V. Sartorelli;J. O’Shea