Xun Zhu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Xun Zhu has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Dong Li
Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China
2 shared publications - Dongmei Yan
Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun City, Jilin Province, China
2 shared publications Mengyan Tang
Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin Province, China
2 shared publicationsZheng Jin
Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin Province, China
2 shared publicationsZhenhua Zhu
Department of Orthopaedic Trauma, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, West of Zhongshan Avenue 183#, Guangzhou, Guangdong Province, China
2 shared publicationsLiping Liu
Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin Province, China
1 shared publication
Latest Publications
- 1 July 2021
- Published by Elsevier in Immunobiology
- Vol. 226 (4) , 152109
Effects of TRIM59 on RAW264.7 macrophage gene expression and function
- 1 July 2021
- Published by Elsevier in Immunobiology
- Vol. 226 (4) , 152109
Effects of TRIM59 on RAW264.7 macrophage gene expression and function
- Open Access
- 18 February 2020
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 11, 263
TRIM59 Protects Mice From Sepsis by Regulating Inflammation and Phagocytosis in Macrophages
Sepsis is associated with bacterial invasion and inflammation and has a high mortality rate. Previous studies have demonstrated that tripartite motif 59 (TRIM59) was involved in NF-κB signaling and could promote phagocytosis of macrophages, but the role of TRIM59 in sepsis is still unknown. In our study, we found that TRIM59 was downregulated in lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs). In the cecal ligation and puncture (CLP) sepsis mice model, the mortality of Trim59flox/floxLyz-Cre (Trim59-cKO) mice was higher, the immune cell infiltration and damage of liver and lung were more severe, and bacteria burden was increased. We also found that TRIM59 altered the production of pro-inflammation cytokines, as well as macrophage phagocytosis ability. Further analysis indicated that NF-κB signal pathway and Fcγ receptors might be involved in these regulations. Our study demonstrated for the first time that TRIM59 protects mice from sepsis by regulating inflammation and phagocytosis in macrophages.
- 18 February 2020
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 11, 263
Open AccessTRIM59 Protects Mice From Sepsis by Regulating Inflammation and Phagocytosis in Macrophages
Sepsis is associated with bacterial invasion and inflammation and has a high mortality rate. Previous studies have demonstrated that tripartite motif 59 (TRIM59) was involved in NF-κB signaling and could promote phagocytosis of macrophages, but the role of TRIM59 in sepsis is still unknown. In our study, we found that TRIM59 was downregulated in lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs). In the cecal ligation and puncture (CLP) sepsis mice model, the mortality of Trim59flox/floxLyz-Cre (Trim59-cKO) mice was higher, the immune cell infiltration and damage of liver and lung were more severe, and bacteria burden was increased. We also found that TRIM59 altered the production of pro-inflammation cytokines, as well as macrophage phagocytosis ability. Further analysis indicated that NF-κB signal pathway and Fcγ receptors might be involved in these regulations. Our study demonstrated for the first time that TRIM59 protects mice from sepsis by regulating inflammation and phagocytosis in macrophages.