Mechanisms of interleukin-6 action in trauma-induced impairment of bone regeneration (C01)

白细胞介素 6 在创伤引起的骨再生损伤中的作用机制 (C01)

• 批准号: 269321693
• 金额: --
• 依托单位: Institut für Unfallchirurgische Forschung und Biomechanik
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2015
• 资助国家: 德国
• 起止时间: 2014-12-31 至 2021-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/269321693?language=en
• 关键词: Mechanisms; interleukin; action; trauma; induced

This project studies the function of interleukin-6 (IL-6) in trauma-induced compromised bone fracture healing. We showed for the first time that IL-6 trans-signaling is non-essential for regular healing, but mediates trauma-induced compromised bone repair, as its selective inhibition led to significantly improved bone healing. By contrast, IL-6 classic signaling induces pro-regenerative effects. We will now further elucidate IL-6-related mechanisms in bone healing with a focus on neutrophils and mast cells, which act as the first line of cellular defense after bone injury and may be the effector and/or target cells of IL-6 signaling.

本课题研究了白介素6(IL-6)在创伤后受损骨折愈合中的作用。我们首次证明了IL-6反式信号转导对正常愈合不是必需的，但介导了创伤诱导的受损的骨修复，因为它的选择性抑制导致了显著的骨愈合改善。相比之下，IL-6经典信号会诱导促再生效应。我们现在将进一步阐明IL-6在骨愈合中的相关机制，重点介绍中性粒细胞和肥大细胞，它们是骨损伤后的第一道细胞防线，可能是IL-6信号转导的效应者和/或靶细胞。