<i>Pseudomonas aeruginosa</i>-induced mitochondrial dysfunction inhibits proinflammatory cytokine secretion and enhances cytotoxicity in mouse macrophages in a reactive oxygen species (ROS)-dependent way.

Haitao Yang; Yan Wang; Hui Fan; Feixue Liu; Huimiao Feng; Xueqing LI; Mingyi Chu; Enzhuang Pan; Daoyang Teng; Huizhen Chen; Jingquan Dong

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Pseudomonas aeruginosa-induced mitochondrial dysfunction inhibits proinflammatory cytokine secretion and enhances cytotoxicity in mouse macrophages in a reactive oxygen species (ROS)-dependent way.

Author: Haitao YANG ¹ ; Yan WANG ² ; Hui FAN ¹ ; Feixue LIU ¹ ; Huimiao FENG ¹ ; Xueqing LI ¹ ; Mingyi CHU ¹ ; Enzhuang PAN ¹ ; Daoyang TENG ¹ ; Huizhen CHEN ³ ; Jingquan DONG ⁴
Author Information

1. Jiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-Industry Technology, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, College of Pharmacy, Jiangsu Ocean University, Lianyungang 222005, China.
2. Department of Medicine Laboratory, the Second People's Hospital of Lianyungang Affiliated to Kangda College of Nanjing Medical University, the Second People's Hospital of Lianyungang City, Lianyungang 222000, China.
3. Institute of Neuroscience, the First People's Hospital of Lianyungang, Lianyungang 222000, China. 2018000029@jou.edu.cn.
4. Jiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-Industry Technology, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, College of Pharmacy, Jiangsu Ocean University, Lianyungang 222005, China. 2018000029@jou.edu.cn.
Publication Type:Journal Article
MeSH: Mice; Animals; Reactive Oxygen Species/metabolism*; Pseudomonas aeruginosa; Macrophages/metabolism*; Mitochondria; Cytokines/metabolism*
From: Journal of Zhejiang University. Science. B 2023;24(11):1027-1036
CountryChina
Language:English
Abstract: 随着铜绿假单胞菌（铜绿）的耐药性逐年增强，铜绿感染已经成为公共医疗卫生的重点关注问题。线粒体自噬及其介导的线粒体功能障碍在多种细菌感染中已被报道，但线粒体功能障碍在宿主调控铜绿感染中的作用尚不明确。因此，本研究建立铜绿刺激小鼠巨噬细胞感染模型和小鼠急性铜绿感染模型，探讨铜绿是否通过诱导线粒体自噬改变线粒体功能，进而影响宿主免疫炎症反应和细胞毒性，并通过监测生存率和肺组织病理学变化进一步确定线粒体自噬在小鼠铜绿体内感染模型中的作用。结果表明，铜绿引起小鼠腹腔巨噬细胞线粒体功能障碍，并通过线粒体自噬途径清除铜绿刺激引起的活性氧（ROS）累积，从而抑制铜绿引起的促炎性细胞因子分泌并增强细胞毒性。体内实验进一步确认线粒体自噬在铜绿体内感染中的作用。