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

作者全名："Zhou, Shouzhi; Yang, Zhao; Liu, Jiaxin; Ran, Maojuan"

作者地址："[Zhou, Shouzhi] Chongqing Med Univ, Yongchuan Hosp, Dept Proctol, Chongqing 402160, Peoples R China; [Yang, Zhao; Liu, Jiaxin; Ran, Maojuan] Chongqing Med Univ, Yongchuan Hosp, Dept Geriatr, Chongqing 402160, Peoples R China"

通信作者："Ran, MJ (通讯作者)，Chongqing Med Univ, Yongchuan Hosp, Dept Geriatr, Chongqing 402160, Peoples R China."

来源：IMMUNOLOGY LETTERS

ESI学科分类：IMMUNOLOGY

WOS号：WOS:000962486500001

JCR分区：Q3

影响因子：3.3

年份：2023

卷号：255

期号：　

开始页：32

结束页：39

文献类型：Article

关键词：TIPE-2; Inflammatory bowel disease; STAT3; NF-kB

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."

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