先天免疫系统
基因工程
脚手架
级联
免疫系统
细胞生物学
免疫学
生物
医学
化学
生物医学工程
基因
遗传学
色谱法
作者
Wenxiao Shi,Yue Feng,Jincheng Tang,Yichang Xu,Wei Wang,Lichen Zhang,Xiaohua Jiang,Zhuang Ding,Kun Xi,Liang Chen,Yun Gu
标识
DOI:10.1002/adhm.202304585
摘要
Abstract The innate immune response is crucial to the inflammation, but how neutrophils and macrophages act in bone repair and tissue engineering treatment strategies await clarification. In this study, we found N2 neutrophils release stronger “eat me” signals to induce macrophage phagocytosis which then polarize into the M2c anti‐inflammatory phenotype. This is beneficial for bone repair. Guided by this biological mechanism, we filled a mesoporous bioactive glass scaffold (MBG) with HAMA hydrogel loaded with TGFβ1 adenovirus (Ad@H), constructing a genetically engineered composite scaffold (Ad@H/M). The scaffold not only has good hydrophilicity and biocompatibility, but also provides mechanical stress support for bone repair. Adenovirus infection quickly induces N2 neutrophils, upregulating NF‐κB and MAPK signaling pathways through Toll‐like receptor 4 (TLR4) to promote the inflammatory response and macrophage phagocytosis. Macrophages perform phagocytosis and polarize towards the M2 phenotype, mediating the inflammatory response by inhibiting the PI3K‐AKT‐NF‐κB pathway, maintaining homeostasis of the osteogenic microenvironment. The role of Ad@H/M scaffold in regulating early inflammation and promoting long‐term bone regeneration was further validated in vivo. In brief, this study focuses on the cascade of reactions between neutrophils and macrophage subtypes, and reports a composite scaffold that coordinates the innate immune response to promote bone repair. This article is protected by copyright. All rights reserved
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