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TRIM21 interacts with IκBα and negatively regulates NF-κB activation in Corynebacterium pseudotuberculosis-infected macrophages

文献类型: 外文期刊

作者: Wu, Chanyu 1 ; Wang, Xiaohan 1 ; Li, Xincan 1 ; Li, Hexian 2 ; Peng, Qiuyue 1 ; Niu, Xiaoxin 1 ; Wu, Yutong 3 ; Wang, Zhiying 1 ; Zhou, Zuoyong 1 ;

作者机构: 1.Southwest Univ, Coll Vet Med, 160 Xueyuan Rd, Chongqing 402460, Peoples R China

2.Sichuan Univ, West China Hosp, State Key Lab Biotherapy & Canc Ctr, Chengdu 610041, Peoples R China

3.Guizhou Acad Agr Sci, Inst Anim Husb & Vet, 1 Laolipo Nanming Dist, Guiyang 550025, Peoples R China

关键词: Corynebacterium pseudotuberculosis; TRIM21; Macrophages; NF-kappa B

期刊名称:VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY ( 影响因子:1.4; 五年影响因子:1.6 )

ISSN: 0165-2427

年卷期: 2025 年 282 卷

页码:

收录情况: SCI

摘要: Corynebacterium pseudotuberculosis, a zoonotic intracellular bacteria, is responsible for abscesses and pyogranuloma formation of the infected host, which is essentially a chronic inflammatory response. Tripartite motif- containing protein 21 (TRIM21) negatively regulates pro-inflammatory cytokines production during C. pseudo- tuberculosis infection, the mechanism of which remains unclear. This study found that C. pseudotuberculosis infection in macrophages induced phosphorylation of I kappa B and p65. TRIM21 interacted with I kappa B alpha by PRY/SPRY domain, stabilizes I kappa B alpha and negatively regulates I kappa B alpha phosphorylation in macrophages during C. pseudotuberculosis infection. In addition, TRIM21 positively regulates the ubiquitination of I kappa B alpha via K48 linkage rather than K63 linkage in C. pseudotuberculosis-infected macrophages. In brief, our research confirmed that TRIM21 negatively regulates canonical NF-kappa B activation by interacting with I kappa B alpha and decreasing I kappa B alpha phosphorylation in macrophages during C. pseudotuberculosis infection. Preventing inflammation induced by C. pseudotuberculosis infection through regulation of the NF-kappa B pathway is a potential way to control this pathogen.

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