生物学杂志

生物学杂志 ›› 2025, Vol. 42 ›› Issue (4): 45-.doi: 10.3969/j.issn.2095-1736.2025.04.045

• 研究报告 • 上一篇    下一篇

绵羊肺炎支原体诱导产生的ROS经MAPK/NLRP3途径对支气管上皮细胞氧化损伤的影响

骆　佳1,2， 徐兆坤1,3， 李雅楠1   

  1. 1. 宁夏大学 生命科学学院 西部特色生物资源保护与利用教育部重点实验室， 银川 750021；
    2. 宁夏医科大学总医院 医学科学研究院， 银川 750004； 3. 宁夏职业技术大学， 银川 750021
  • 出版日期:2025-08-18 发布日期:2025-08-13
  • 通讯作者: 李雅楠，博士，副教授，研究方向为病原微生物，E-mail:lyn@nxu.edu.cn
  • 作者简介:骆佳，博士，副教授，研究方向为病原微生物，E-mail:sophia.lou@foxmail.com
  • 基金资助:
    宁夏回族自治区重点研发项目（引才专项）（2019BEB04013）

Effect of Mycoplasma ovipneumoniae-induced ROS mediated oxidative damage through MAPK/NLRP3 signaling in sheep bronchial epithelial cells

LUO Jia1,2, XU Zhaokun1,3, LI Ya’nan1   

  1. 1. Key Laboratory of Ministry of Education for Conservation and Utilization of Special Biological Resources in the
    Western China, College of Life Science, Ningxia University, Yinchuan 750021, China; 2. Institute of Medical Sciences,
    General Hospital of Ningxia Medical University, Yinchuan 750004, China; 3. Ningxia Polytechnic University,
    Yinchuan 750021, China
  • Online:2025-08-18 Published:2025-08-13

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摘要： 采用气液相（air-liquid interface，ALI）培养方式构建支气管原代上皮细胞（宁夏滩羊）模型，探讨绵羊肺炎支原体（Mycoplasma ovipneumoniae）诱导产生的活性氧（ROS）对支气管上皮细胞氧化损伤的作用机制。结果表明，M. ovipneumoniae诱导产生的ROS通过激活MAPK（ERK、JNK、p38 MAPK）信号通路，活化炎症小体NLRP3，释放炎症因子，引发凋亡。同时，NLRP3炎症复合小体装配过程中所激活的caspase-1可提高MAPK的活化效率，加强NLRP3的活化，从而形成一个正反馈回路。结果显示，M. ovipneumoniae诱导产生的ROS经MAPK/NLRP3信号介导的氧化损伤在M. ovipneumoniae感染的支气管上皮细胞的发病过程中发挥重要的调节作用。

关键词: 绵羊肺炎支原体, 支气管上皮细胞, 气液相界面, NLRP3, 氧化损伤

Abstract: In this study, the impacts ofMycoplasma ovipneumoniae-induced ROS on oxidative damage were analyzed in primary bronchial epithelial cells (Ovis aries, Ningxia Tan sheep ) which were used to obtain an air-liquid interface ( ALI ) epithelial culture model. The results indicated thatM. ovipneumoniae-induced ROS production led to the release of inflammatory factors and initiation of apoptosis through activating MAPK ( ERK, JNK and p38 MAPK ) signaling-mediated NLRP3 signaling pathways. Meanwhile, during the NLRP3 inflammasome assembly, the activated caspase-1 improved the efficiency of activation of MAPK and forming a positive feedback loop. These data suggested thatM. ovipneumoniae-induced ROS production played an important regulatory role in the cellular pathogenesis ofM. ovipneumoniae-infected sheep bronchial epithelial cells through MAPK/NLRP3 signaling.

Key words: Mycoplasma ovipneumoniae, bronchial epithelial cells, air-liquid interface, NLRP3, oxidative damage

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