肠道上皮质和髓状免疫细胞形成结肠炎严重程度和结肠直肠癌通过高流动性组盒蛋白1形成
Katharina Foelsch1, Penelope Pelczar1, Elisabeth Zierz1
1Department of Internal Medicine, I. Medical Clinic and Polyclinic, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Journal of Crohn's & colitis
|January 29, 2024
概括
肠细胞和髓质细胞中的高流动性组盒蛋白1 (HMGB1) 根据环境,调节对结肠炎和结肠直肠癌 (CRC) 的反应. 根据细胞类型和疾病背景,HMGB1的作用有所不同,影响宿主反应和肠道愈合.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 高流动性组盒子蛋白1 (HMGB1) 是一种核蛋白,在炎症期间参与免疫调节.
- HMGB1水平与结肠炎的严重程度和结肠直肠癌 (CRC) 的进展相关.
- 在结肠炎期间HMGB1在肠细胞命运中的细胞内作用及其在CRC中的功能需要进一步调查.
研究的目的:
- 研究HMGB1在结肠炎和结肠炎相关的CRC的不同情境中的功能.
- 探索HMGB1在肠细胞和髓状细胞在肠道炎症和癌症中的作用.
主要方法:
- 在肠细胞 (Hmgb1ΔIEC) 和髓状细胞 (Hmgb1ΔLysM) 中使用了有条件的HMGB1淘汰赛的小鼠.
- 研究了HMGB1在化学诱导的大肠炎,Citrobacter rodentium大肠炎,T细胞转移大肠炎以及Apc+/min CRC模型中的作用.
- 评估了肠细胞和有机体功能,体内重编程和癌症表型.
主要成果:
- 在人类炎症性肠病和胃肠道癌症中,HMGB1过度表达.
- 肠细胞HMGB1缺陷加剧了化学诱导的肠损伤,但不是其他大肠炎模型.
- 肠细胞中的HMGB1缺乏并没有改变细胞内在功能,但影响了体内重编程,并增加了CRC负担.
- 骨髓细胞中的HMGB1缺陷减弱了炎症性CRC.
- HMGB1以情境依赖的方式调节免疫信号和细胞外矩阵重塑.
结论:
- 肠细胞和髓质细胞通过HMGB1.1差异调节宿主对结肠炎和肠道伤口愈合的反应.
- HMGB1在肠道炎症和CRC发育中发挥着上下文依赖的作用.
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