Toll-Like Receptor 4 Exacerbates Mycoplasma pneumoniaevia Promoting Transcription Factor EB-Mediated Autophagy

被引:1
|
作者
Liu, Yan [1 ]
Li, Jing [1 ]
Lu, Xianfeng [1 ]
Zhen, Shuangping [1 ]
Huo, Jing [1 ]
机构
[1] Shanxi Prov Peoples Hosp, Pediat Dept, Taiyuan 030014, Shanxi, Peoples R China
关键词
IMMUNE-RESPONSE; GAUCHER-DISEASE; INFECTION; TFEB; THERAPY;
D O I
10.1155/2022/3357694
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Mycoplasma pneumoniae (M. pneumoniae) is the most common cause of community-acquired pneumonia. Toll-like receptors (TLRs) play an essential role in pneumonia. The purpose of this study was to investigate the roles of TLR4 in M. pneumoniae. Mice were administrated with 100 mu l (1 x 107 ccu/ml) of M. pneumoniae. HE staining was applied for histological analysis. The protein expression was determined by western blot. The cytokine level was detected by ELISA. The results showed that TLR4-deficient mice were protected from M. pneumoniae. However, downregulation of TLR4 inhibited inflammatory response and autophagy. Moreover, transcription factor EB (TFEB) participated in M. pneumoniae-induced inflammatory response and autophagy, while knockdown of TLR4 downregulated TFEB and its nuclear translocation.
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页数:9
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