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由骨细胞陷窝-小管网络介导的免疫逃逸导致持续性和无法治愈的骨感染。

Immune escape of mediated by osteocyte lacuna-canalicular network leads to persistent and uncured bone infection.

作者信息

Rong Zhigang, Chen Xiaozhen, Qin Leilei, Wang Xiaohua, Luo Fei, Zou Quanming, Zeng Hao

机构信息

Department of Orthopaedics, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.

National Engineering Research Center of Immunological Products, Third Military Medical University (Army Medical University), Chongqing, China.

出版信息

Front Cell Infect Microbiol. 2025 Jun 2;15:1592086. doi: 10.3389/fcimb.2025.1592086. eCollection 2025.

Abstract

Bone infections, specifically chronic osteomyelitis, are characterized by recurrent episodes. They are considered intractable clinical diseases as they require protracted and difficult-to-cure courses. () is the most common pathogen responsible for bone infections and has high destruction rates. Previous literature has indicated that during osteomyelitis, immune evasion mainly involves three mechanisms: biofilm formation, intracellular infection, and abscess formation. However, recently, it was observed that can enter and persist for a long time in the Osteocyte lacuno-canalicular network (OLCN), a bone microstructure. Furthermore, it has been found to successfully evade the host's immune system natural physical barriers, chemical properties, and bone microstructure's immune escape mechanisms. Therefore, bone infections are more difficult to cure than soft-tissue infections. Currently, there are only a few studies on OLCN invasion by , and the clinical evidence is not sufficient. Therefore, this review aimed to combine relevant published literature on the OLCN-mediated immune escape of to elaborate on the pathological mechanisms associated with protracted and difficult-to-cure bone infections. The findings will provide a scientific basis and theoretical foundation for future comprehensive analysis of how invades OLCN and novel treatment strategies for bone infections.

摘要

骨感染,特别是慢性骨髓炎,其特征为反复发作。它们被认为是难治性临床疾病,因为其病程漫长且难以治愈。()是导致骨感染最常见的病原体,且具有高破坏率。先前的文献表明,在骨髓炎期间,免疫逃逸主要涉及三种机制:生物膜形成、细胞内感染和脓肿形成。然而,最近观察到()能够进入骨微结构骨细胞陷窝-小管网络(OLCN)并在其中长期存留。此外,已发现它能成功避开宿主免疫系统的天然物理屏障、化学特性以及骨微结构的免疫逃逸机制。因此,骨感染比软组织感染更难治愈。目前,关于()对OLCN侵袭的研究较少,临床证据也不充分。因此,本综述旨在结合已发表的关于()通过OLCN介导免疫逃逸的相关文献,阐述与骨感染病程漫长且难以治愈相关的病理机制。这些发现将为未来全面分析()如何侵袭OLCN以及骨感染的新治疗策略提供科学依据和理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd55/12171435/48dcd0593d05/fcimb-15-1592086-g001.jpg

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