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Long non-coding RNA MMTP mediates necroptosis in alveolar macrophages during Mycoplasma hyopneumoniae infection by enhancing TNF-α transcription

文献类型： 外文期刊

作者： Zhang, Zhenzhen 1 ; Mei, Xiuzhen 1 ; Wang, Hui 1 ; Gong, Hanfei 1 ; Chen, Rong 1 ; Liu, Beibei 1 ; Wei, Yanna 1 ; Gan, Yuan 1 ; Yuan, Ting 1 ; Wu, Yuzi 1 ; Shao, Guoqing 1 ; Xiong, Qiyan 1 ; Zhang, Chao 1 ; Feng, Zhixin 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing 210014, Peoples R China

2.GuoTai Taizhou Ctr Technol Innovat Vet Biol, Taizhou 225300, Peoples R China

3.Nanjing Agr Univ, Sch Anim Med, Nanjing 210095, Peoples R China

4.Nanjing Normal Univ, Coll Marine Sci & Engn, Jiangsu Key Lab Aquat Crustacean Dis, Nanjing 210023, Peoples R China

5.China Pharmaceut Univ, Sch Tradit Chinese Pharm, Nanjing 210009, Peoples R China

关键词： mycoplasma pneumonia; lncRNA; necroptosis

期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：8.5； 五年影响因子：8.7 ）

ISSN： 0141-8130

年卷期： 2025 年 288 卷

页码：

收录情况： SCI

摘要： Mycoplasma hyopneumoniae (M. hyo), a major respiratory pathogen in swine, causes chronic respiratory diseases characterized by severe lung inflammation. Alveolar macrophages, which serve as the first line of defense in the respiratory immune system, undergo necroptosis in response to M. hyo infection. This form of programmed cell death amplifies pulmonary inflammation and leads to impaired lung function, yet the precise molecular mechanisms remain poorly understood. Long non-coding RNAs (lncRNAs), known for their regulatory roles in transcriptional and epigenetic processes, have been linked to various inflammatory and infectious diseases. In this study, we identified a novel lncRNA, lncRNA-MMTP, as a critical regulator of necroptosis during M. hyo infection. Mechanistically, lncRNA-MMTP interacts with the transcription factor TFII-I to enhance c-Fos promoter activity, leading to increased transcription of TNF-alpha and activation of the RIPK1/RIPK3/MLKL necroptotic pathway. Importantly, knockdown of lncRNA-MMTP or inhibition of TFII-I significantly reduced TNF-alpha levels and necroptosis in alveolar macrophages. These findings not only elucidate a new molecular pathway underlying M. hyo-induced lung inflammation but also suggest potential therapeutic targets for managing pathogen-induced inflammatory responses in the respiratory system.

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