肥胖会延长促炎反应,并减弱植入物上的骨愈合
Derek Avery1, Lais Morandini1, Luke Sheakley1
1Department of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, Richmond, VA, United States.
Acta biomaterialia
|November 25, 2024
概括
肥胖症通过促进慢性炎症和改变免疫细胞反应,损害了植入物周围的骨形成. 这导致肥胖个体的生物材料整合和愈合减少.
科学领域:
- 生物材料科学 生物材料科学
- 免疫学 免疫学 免疫学
- 代谢性疾病研究研究
背景情况:
- 肥胖是一种代谢性疾病,其特点是慢性系统性炎症.
- 肥胖会影响免疫细胞的功能,增加促炎性细胞因子.
- 生物材料的表面特性会影响植入部位的免疫细胞行为.
研究的目的:
- 为了研究饮食诱导的肥胖对改性 (Ti) 植入物的炎症反应的影响.
- 评估肥胖对植入周边免疫细胞群和骨形成的影响.
- 确定肥胖如何影响免疫细胞表型和功能在周围植入物微环境.
主要方法:
- 在使用高脂肪饮食 (HFD) 的小鼠中诱导肥胖.
- 对周围植入物免疫细胞透的分析 (中性粒细胞,巨细胞,T细胞,MSCs).
- 测量循环中的阿迪波金和促炎性细胞因子.
- 评估Ti植入物周围的骨形成.
- 从肥胖的小鼠转移到瘦小鼠的骨髓细胞.
主要成果:
- 肥胖小鼠的中性粒细胞,促炎性巨细胞和T细胞增加,而Ti植入物周围的抗炎性巨细胞和MSCs减少.
- 肥胖导致循环阿迪波金和促炎细胞因子的升高.
- 在肥胖小鼠中,Ti植入物周围的骨形成显著减少.
- 收养转移证实了肥胖在促进有利于炎症的植入周围环境和损害骨愈合中的作用.
结论:
- 肥胖症显著改变了对修改的Ti植入物的免疫反应,延长了炎症.
- 肥胖会影响植入周围骨的形成和生物材料的整合.
- 饮食引起的肥胖会产生一种促炎性微环境,阻碍骨质整合.
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