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Francisella novicida Mutant XWK4 Triggers Robust Inflammasome Activation Favoring Infection.

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机构: [1]School of Life Sciences, University of Science and Technology of China, Hefei, China. [2]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China. [3]Key Laboratory for Experimental Teratology of the Ministry of Education, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China. [4]State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China. [5]Department of Clinical Laboratory,The First Affiliated Hospital of Kunming Medical University,Kunming,China. [6]Yunnan Key Laboratory of Laboratory Medicine, Kunming, China. [7]Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
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关键词: Francisella novicida XWK4 AIM2 NLRP3 ASC

摘要:
Bacterial infection tendentiously triggers inflammasome activation, whereas the roles of inflammasome activation in host defense against diverse infections remain unclear. Here, we identified that an ASC-dependent inflammasome activation played opposite roles in host defense against Francisella novicida wild-type (WT) U112 and mutant strain XWK4. Comparing with U112, XWK4 infection induced robust cytokine production, ASC-dependent inflammasome activation, and pyroptosis. Both AIM2 and NLRP3 were involved and played independent roles in XWK4-induced inflammasome activation. Type II interferon was partially required for XWK4-triggered inflammasome activation, which was different from type I interferon dependency in U112-induced inflammasome activation. Distinct from F. novicida U112 and Acinetobacter baumannii infection, Asc-/- mice were more resistant than WT mice response to XWK4 infection by limiting bacterial burden in vivo. The excessive inflammasome activation triggered by XWK4 infection caused dramatical cell death and pathological damage. Our study offers novel insights into mechanisms of inflammasome activation in host defense and provides potential therapeutic approach against bacterial infections and inflammatory diseases.Copyright © 2021 Guo, Mao, Xie, Cheng, Xu, Wang, Du and Qi.

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出版当年[2022]版:
大类 | 2 区 生物学
小类 | 2 区 发育生物学 3 区 细胞生物学
最新[2023]版:
大类 | 2 区 生物学
小类 | 2 区 发育生物学 3 区 细胞生物学
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出版当年[2021]版:
Q1 DEVELOPMENTAL BIOLOGY Q2 CELL BIOLOGY
最新[2023]版:
Q1 DEVELOPMENTAL BIOLOGY Q2 CELL BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

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第一作者机构: [1]School of Life Sciences, University of Science and Technology of China, Hefei, China. [2]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China.
通讯作者:
通讯机构: [2]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China. [3]Key Laboratory for Experimental Teratology of the Ministry of Education, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China. [5]Department of Clinical Laboratory,The First Affiliated Hospital of Kunming Medical University,Kunming,China. [6]Yunnan Key Laboratory of Laboratory Medicine, Kunming, China. [7]Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
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