准骨髓 FoxO1 通过调节 Tim4+ 巨细胞糖解来改善败血症引起的肠道损伤
Jiali Ni1,2, Ruowen Zhang1,2, Yaqi Pu3
1The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, PR China.
叉头盒O1 (FoxO1) 调节了败血症的炎症反应. 在髓状细胞中抑制FoxO1通过促进抗炎性巨细胞来保护肠道受伤,从而提供了一个新的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 胃肠病学 胃肠病学
背景情况:
- 败血症引起的肠损伤是一种与巨细胞功能障碍相关的严重并发症.
- 转录因子Forkhead Box O1 (FoxO1) 在这个过程中的作用尚不清楚.
研究的目的:
- 为了研究骨髓 FoxO1 在败血症引起的肠损伤中的功能.
- 为了确定FoxO1作为这种情况的潜在治疗目标.
主要方法:
- 利用骨髓细胞特异性FoxO1条件淘汰 (FoxO1M-KO) 的小鼠来研究败血症.
- 分析了巨细胞群,肠道屏障功能,氧化应激和炎症标志物.
- 研究了涉及FoxO1,Sin3a,Tim4和MAP4K4信号的分子机制.
- 评估了华夏百度配方 (HSBD) 的治疗潜力.
主要成果:
- 在败血症期间,肠道巨细胞的FoxO1表达被上调.
- 骨髓细胞中的FoxO1缺失减轻了肠道损伤,改善了屏障功能,并减少了氧化应激和全身炎症.
- FoxO1 缺乏增加了 Tim4+ 寄宿性巨细胞,通过 MAP4K4 信号抑制了葡萄糖分解,并产生抗炎作用.
- 收养转移实验证实了FoxO1-调节的Tim4+巨细胞的关键作用.
- 治疗HSBD抑制了FoxO1并改善了败血性肠损伤.
结论:
- 骨髓 FoxO1 在败血症引起的肠损伤中起着至关重要的免疫调节作用.
- 准FoxO1,特别是在Tim4+巨细胞内,代表了治疗败血症的新治疗策略.
- 传统中医HSBD通过调节FoxO1.1来减轻这种情况的潜力.
更多相关视频
07:05Fluorescence-mediated Tomography for the Detection and Quantification of Macrophage-related Murine Intestinal Inflammation
Published on: December 15, 2017
10:21Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
Published on: September 12, 2019
相关概念视频
Regulation of Angiogenesis and Blood Supply
Liver Regeneration
Cells of Liver
The liver comprises four major types of cells— hepatocytes, stellate, Kupffer, and sinusoidal endothelial cells. The hepatocytes are large...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Hormones Regulating Blood Glucose
In addition to accelerating glucose uptake and utilization, insulin has...
Glucose Homeostasis: Regulation of Blood Glucose
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
Type I Diabetes II: Pathophysiology
