在慢性炎症期间有机感应反循环
Sarbari Saha1,2,3, Dafne Müller1, Andrew G Clark1,2,3
1University of Stuttgart, Institute of Cell Biology and Immunology, Stuttgart, Germany.
Frontiers in cell and developmental biology
|July 26, 2023
概括
表皮屏障的破坏会改变组织机制,促进炎症. 针对这些机械变化提供了治疗慢性炎症疾病的新策略,如炎症性肠病 (IBD).
科学领域:
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
- 生物物理学的生物物理.
背景情况:
- 表皮组织在皮肤,肺部和肠道等器官中形成关键屏障,防止感染.
- 障碍物破坏会引发炎症,但相关的组织力学变化往往被忽视.
研究的目的:
- 审查将上皮质屏障功能障碍与组织机械变化联系起来的分子机制.
- 探索这些机械变化如何影响免疫反应和疾病进展.
主要方法:
- 文献综述侧重于分子机制.
- 对直接 (ECM酶分泌) 和间接 (纤维细胞激活) 途径的分析.
- 讨论屏障功能与机械之间的反循环.
主要成果:
- 表皮屏障的损失直接和间接地改变了组织机制.
- 改变的机制调节免疫细胞的活动并加剧炎症.
- 在屏障功能障碍和机械变化之间存在正反循环.
结论:
- 组织机械变化是表皮屏障破坏和慢性炎症的组成部分.
- 调节组织力学为炎症性疾病提供了一个新的治疗框架.
- 这一框架与炎症性肠病 (IBD),肝病和癌症有关.
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