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Mycoplasma hyopneumoniae Infection Activates the NOD1 Signaling Pathway to Modulate Inflammation

文献类型: 外文期刊

作者: Liu, Wei 1 ; Jiang, Pengcheng 1 ; Yang, Keli 1 ; Song, Qiqi 3 ; Yuan, Fangyan 1 ; Liu, Zewen 1 ; Gao, Ting 1 ; Zhou, Danna 1 ; Guo, Rui 1 ; Li, Chang 1 ; Sun, Pei 2 ; Tian, Yongxiang 1 ;

作者机构: 1.Hubei Acad Agr Sci, Inst Anim Husb & Vet Sci, Key Lab Prevent & Control Agents Anim Bacteriosis, Hubei Prov Key Lab Anim Pathogen Microbiol,Minist, Wuhan, Peoples R China

2.Anhui Agr Univ, Coll Anim Sci & Technol, Anhui Prov Key Lab Vet Pathobiol & Dis Control, Hefei, Peoples R China

3.Tianjin Agr Univ, Coll Anim Sci & Vet Med, Tianjin Key Lab Agr Anim Breeding & Hlth Husb, Tianjin, Peoples R China

关键词: Mycoplasma hyopneumoniae; mhp390; NOD1; inflammation; interaction

期刊名称:FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY ( 影响因子:6.073; 五年影响因子:6.34 )

ISSN: 2235-2988

年卷期: 2022 年 12 卷

页码:

收录情况: SCI

摘要: Mycoplasma hyopneumoniae is a highly contagious pathogen causing porcine enzootic pneumonia, which elicits prolonged inflammatory response modulated by pattern recognition receptors (PRRs). Although significant advances have been achieved in understanding the Toll-Like receptors that recognize M. hyopneumoniae, the role of nucleotide-binding oligomerization domain 1 (NOD1) in M. hyopneumoniae infected cells remains poorly understood. This study revealed that M. hyopneumoniae activates the NOD1-RIP2 pathway and is co-localized with host NOD1 during infection. siRNA knockdown of NOD1 significantly impaired the TRIF and MYD88 pathway and blocked the activation of TNF-alpha. In contrast, NOD1 overexpression significantly suppressed M. hyopneumoniae proliferation. Furthermore, we for the first time investigated the interaction between M. hyopneumoniae mhp390 and NOD1 receptor, and the results suggested that mhp390 and NOD1 are possibly involved in the recognition of M. hyopneumoniae. These findings may improve our understanding of the interaction between PRRs and M. hyopneumoniae and the function of NOD1 in host defense against M. hyopneumoniae infection.

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