JCC: IL-6缺失会加剧IL-10缺乏小鼠的结肠炎并诱发全身性炎症反应

2020-07-12 MedSci原创 MedSci原创

白介素6 [IL-6]或其受体目前是炎症性肠病[IBD]靶向生物治疗的候选目标。

背景和目标

白介素6 [IL-6]或其受体目前是炎症性肠病[IBD]靶向生物治疗的候选目标。因此,必须全面了解阻断IL-6的效果。本项研究旨在通过评估IL-6缺失对IL-10-缺陷小鼠[IL-10 -/- ] 自发性结肠炎的影响进行了探究。

 

方法

研究人员将产生IL-6 / IL-10双缺陷[IL-6 -/- / IL-10 -/- ]小鼠与野生型相比结肠粘膜的肠道炎症。

 

结果

出乎意料的是,IL-6 -/- / IL-10 -/-小鼠表现出比IL-10 -/-小鼠更明显的肠道炎症和更早的疾病发作,无论是局部[结肠和小肠]还是全身性[脾肿大,溃疡性皮炎] ,白细胞增多,中性粒细胞增多和单核细胞增多]。IL-6 -/- / IL-10 -/-小鼠表现出多种细胞因子[IL-1β,IL-4,IL-12,TNFα]和趋化因子[MCP-1和MIG]的升高,但IFN-γ没有升高。

 

结论

在IL-10 -/-小鼠可以部分通过抑制Treg / CTLA-4并促进IL-1β/ Th2途径,完全IL-6阻断可显着加重肠道炎症。另外,双重突变体表现出严重的全身性炎症的迹象。

 

原始出处:

Mei Ye. Et al. Deletion of IL-6 Exacerbates Colitis and Induces Systemic Inflammation in IL-10-Deficient Mice. Journal of Crohn's and Colitis. 2020.

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    2020-07-14 kzlchina
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    2020-07-14 jjjiang0202
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