RIPK2的泛素化是由Peli3介导的,并负向调控感染性骨髓炎的发生。

IF 1.3 4区 医学 Q4 INFECTIOUS DISEASES Japanese journal of infectious diseases Pub Date : 2023-07-24 DOI:10.7883/yoken.JJID.2022.622
Lixiang Le, Haojie Shan, Yiwei Lin, Wenyang Xia, Xin Ma, Chaolai Jiang, Zhongmin Shi, Youjia Xu
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引用次数: 0

摘要

骨髓炎是对骨骼的感染和破坏。到目前为止,还没有通用的治疗方案。受体相互作用丝氨酸/苏氨酸蛋白激酶2 (RIPK2)与骨髓炎的发展有关。然而,其具体机制尚不清楚。本研究采用6-8w野生型或Pellino E3泛素蛋白连接酶家族成员3 (Peli3)缺陷小鼠注射金黄色葡萄球菌诱导骨髓炎。用脂多糖(LPS)处理小鼠RAW264.7细胞或骨髓源性巨噬细胞。在LPS刺激后,RAW264.7细胞中敲低Peli3可增加炎症因子(白细胞介素-1β、白细胞介素-6和肿瘤坏死因子-α)的表达。金黄色葡萄球菌诱导的peli3缺陷小鼠的炎症也被激活。此外,金黄色葡萄球菌感染的peli3缺陷小鼠比金黄色葡萄球菌感染的野生型小鼠表现出更严重的骨髓炎症状。此外,Peli3通过k48相关的泛素化作用靶向并降解RIPK2,并通过降解RIPK2负向调节骨髓炎。我们的数据进一步扩展了目前对RIPK2在骨髓炎中的理解,并表明RIPK2可能作为治疗骨髓炎的新靶点。
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The Ubiquitination of RIPK2 is Mediated by Peli3 and Negatively Regulates the Onset of Infectious Osteomyelitis.

Osteomyelitis is the infection and destruction of the bone. To date, there is no universal protocol for its treatment. Receptor-interacting serine/threonine-protein kinase 2 (RIPK2) has been implicated in osteomyelitis development. However, the detailed mechanism remains unknown. Here, 6-8w wild-type or Pellino E3 Ubiquitin Protein Ligase Family Member 3 (Peli3)-deficient mice were injected with Staphylococcus aureus to induce osteomyelitis. RAW264.7 cells or bone marrow-derived macrophages isolated from mice were treated with lipopolysaccharide (LPS). Knocking down Peli3 in RAW264.7 cells increased the expression of inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) after LPS stimulation. Inflammation was also activated in S. aureus-induced Peli3-deficient mice. Moreover, S. aureus-infected Peli3-deficient mice also displayed more severe symptoms of osteomyelitis than S. aureus-infected wild-type mice. Moreover, Peli3 targets and degrades RIPK2 through K48-linked ubiquitination, and negatively modulates osteomyelitis by degrading RIPK2. Our data further expands the current understanding of RIPK2 in osteomyelitis, and suggests that RIPK2 might serve as a novel therapeutic target for treating osteomyelitis.

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来源期刊
CiteScore
4.50
自引率
4.50%
发文量
172
审稿时长
2 months
期刊介绍: Japanese Journal of Infectious Diseases (JJID), an official bimonthly publication of National Institute of Infectious Diseases, Japan, publishes papers dealing with basic research on infectious diseases relevant to humans in the fields of bacteriology, virology, mycology, parasitology, medical entomology, vaccinology, and toxinology. Pathology, immunology, biochemistry, and blood safety related to microbial pathogens are among the fields covered. Sections include: original papers, short communications, epidemiological reports, methods, laboratory and epidemiology communications, letters to the editor, and reviews.
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