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Mycoplasma ovipnuemoniae impairs the immune response of sheep and suppresses neutrophil function by inhibiting S100A9

文献类型： 外文期刊

作者： Yan, Chenbo 1 ; Dong, Tianning 1 ; Shan, Yiyi 2 ; Zhao, Bingru 1 ; Yang, Hua 1 ; Cai, Yu 1 ; Li, Shanglai 1 ; Liu, Qiuyue 3 ; Chu, Yuefeng 4 ; Hao, Huafang 4 ; Cheng, Zilong 2 ; Liu, Maojun 1 ; Zhang, Yanli 1 ;

作者机构： 1.Nanjing Agr Univ, Jiangsu Livestock Embryo Engn Lab, Nanjing 210095, Peoples R China

2.Jiangsu Acad Agr Sci, Inst Vet Med, Key Lab Vet Biol Engn & Technol, Minist Agr, Nanjing 210014, Peoples R China

3.Chinese Acad Sci, Inst Genet & Dev Biol, State Key Lab Mol Dev Biol, Beijing 100101, Peoples R China

4.Lanzhou Univ, Lanzhou Vet Res Inst, Chinese Acad Agr Sci, State Key Lab Anim Dis Control & Prevent,Coll Vet, Lanzhou 730000, Peoples R China

关键词： Sheep; Mycoplasma ovipneumoniae; ScRNA-seq; Neutrophils

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：2.7； 五年影响因子：2.9 ）

ISSN： 0378-1135

年卷期： 2025 年 303 卷

页码：

收录情况： SCI

摘要： Mycoplasma pneumonia is a chronic respiratory disease that seriously affects the health of sheep. To date, little information is available about the damage caused by Mycoplasma ovipneumoniae (MO) pneumonia to host lungs. Here, after sheep were infected with MO for 28 days, severe inflammatory reactions and pathological damage occurred. By using single-cell RNA sequencing (scRNA-seq), all the transcriptome changes in 11 cell types in sheep lung tissue were systematically analyzed, and the key biological processes regulating inflammation and immunity were identified. Moreover, we constructed both intercellular communication models and differential expression maps of key regulatory genes for each cell subgroup. We also specifically focused on the response of T cell subpopulations and neutrophils to MO infection. Long-term infection may affect an organism's immune response, inhibit intercellular communication, and highlight the important role of the cyclophilin A (CypA) and macrophage migration inhibitory factor (MIF) pathways in intercellular communication. Notably, MO infection decreased the toxicity of CD8 effector T cells and depleted regulatory T cells, thus inhibiting normal cell function. Subsequently, emphasis was placed on the important role of the neutrophil marker gene S100A9 in promoting neutrophil clearance of MO through activation of the ERK signaling pathway and reactive oxygen species (ROS) burst in vitro. These results contribute to understanding the progression of MO infection in the lungs and provide a rich database on the molecular basis of the response to different cell types in MO infection.

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