TIPE-2 ameliorates inflammatory bowel disease in mice via inhibiting STAT3 and NF-kB activation

被引：4
|
作者：
Zhou, Shouzhi [1 ]
Yang, Zhao [2 ]
Liu, Jiaxin [2 ]
Ran, Maojuan [2 ]
机构：
[1] Chongqing Med Univ, Yongchuan Hosp, Dept Proctol, Chongqing 402160, Peoples R China
[2] Chongqing Med Univ, Yongchuan Hosp, Dept Geriatr, Chongqing 402160, Peoples R China
来源：
IMMUNOLOGY LETTERS | 2023年 / 255卷
关键词：
TIPE-2; Inflammatory bowel disease; STAT3; NF-kB; NEGATIVE REGULATOR; GUT MICROBIOTA; IMMUNITY; EXPRESSION; RESPONSES; TNFAIP8; INNATE;
D O I：
10.1016/j.imlet.2023.02.005
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
TIPE-2 has been identified as a negative regulator of both innate and adaptive immunity and is involved in several inflammatory diseases. However, the immune inhibition mechanism of TIPE-2 involved in inflammatory bowel disease has not been well studied. Therefore, the aim of this study was to investigate whether TIPE-2 improved experimental colitis by reducing high levels of inflammation in the intestine. Lentivirus encoding TIPE-2 was administered to mice by intrarectal injection after colitis induction. Histological analysis was used to analyze sections of the intestine. Protein expression induced by STAT3 and NF-kappa B signaling was analyzed by western blot. We found that TIPE-2 reduced the colitis activity index score and the histological score of the intestine. TIPE-2 also decreased inflammatory cytokine levels in the intestine. Additionally, TIPE-2 inhibited STAT3 and NF-kB activation. These results suggested that TIPE-2 might attenuate inflammation of colitis via inhibiting of STAT3 and NF-kB activation.
引用
收藏
页码：32 / 39
页数：8
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