一氧化碳诱导的自增强了通过对膜作用在小鼠多微生物败血症中增强人类介质体细胞功能
Narae Hwang1, Sailaja Ghanta2, Qifei Li3
1Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
概括
一氧化碳 (CO) 通过诱导自增强了对血症的介酶体 stromal cell (MSC) 疗法. 这改善了细菌清除,并通过修改的细胞外囊泡减少了器官损伤,提供了一种新的败血症治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 再生医学是一种再生医学.
背景情况:
- 败血症是一种具有高死亡率的严重疾病,需要先进的治疗策略.
- 介质细胞 stromal 细胞 (MSCs) 显示出治疗败血症的希望,但它们的疗效可以通过调节来提高.
- 一氧化碳 (CO) 以其细胞保护作用和调节炎症和自的能力而闻名.
研究的目的:
- 调查CO诱导的自在人类MSCs (hMSCs) 中的作用,以治疗败血症.
- 在小鼠模型中确定CO条件hMSCs对败血症结局的影响.
- 阐明CO介导的hMSC功能的增强背后的机制,重点关注细胞外囊泡 (EV) 和它们的miRNA载荷.
主要方法:
- 在hMSC中,使用CO的条件是ex vivo.
- 对CO-条件hMSCs的功能效应进行了评估,用于毒症的小鼠模型 (结和刺穿).
- 在体外测试中评估了中性粒细胞细胞,巨细胞细胞,以及自抑制和miRNA操纵的作用.
主要成果:
- 氧化碳调节增强了hMSC存活率,体内细菌清除和体内中性粒细胞化.
- 氧化碳治疗导致中性粒细胞透和对细胞死亡减少,与巨细胞增多相关.
- 二氧化碳的有益作用依赖于自,并通过EVs内的改变的miRNA载荷 (miR-145-3p,miR-193a-3p) 来调节.
结论:
- CO诱导的自增强了hMSCs在败血症中的治疗潜力.
- 由MSC衍生的EV在通过特定的miRNA调制来调解CO的保护作用方面发挥着至关重要的作用.
- 这项研究突出了通过利用CO诱导的自和EV介导的膜信号传递来改善基于MSC的败血症治疗的新策略.
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