Zhou Shouzhi, Yang Zhao, Liu Jiaxin, Ran Maojuan
Department of Proctology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Department of Geriatrics, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Immunol Lett. 2023 Mar;255:32-39. doi: 10.1016/j.imlet.2023.02.005. Epub 2023 Feb 26.
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-κB 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.
TIPE-2已被确定为先天性和适应性免疫的负调节因子，并参与多种炎症性疾病。然而，TIPE-2参与炎症性肠病的免疫抑制机制尚未得到充分研究。因此，本研究的目的是探讨TIPE-2是否通过降低肠道高水平炎症来改善实验性结肠炎。在诱导结肠炎后，通过直肠内注射将编码TIPE-2的慢病毒给予小鼠。用组织学分析来分析肠道切片。通过蛋白质印迹法分析由STAT3和NF-κB信号诱导的蛋白质表达。我们发现TIPE-2降低了结肠炎活动指数评分和肠道组织学评分。TIPE-2还降低了肠道中炎性细胞因子水平。此外，TIPE-2抑制STAT3和NF-κB的激活。这些结果表明，TIPE-2可能通过抑制STAT3和NF-κB的激活来减轻结肠炎的炎症。
