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2 results on '"Chaoxiong Yue"'

1. Autophagy Is a Defense Mechanism Inhibiting Invasion and Inflammation During High-Virulent Haemophilus parasuis Infection in PK-15 Cells

Author

Chaoxiong Yue, Jinquan Li, Hui Jin, Kexin Hua, Wei Zhou, Yueyi Wang, Guirong Cheng, Dan Liu, Lang Xu, Yushan Chen, and Yan Zeng

Subjects
Haemophilus parasuis, SH0165, autophagy, invasion, inflammation, Microbiology, QR1-502
Abstract

Bacterial infections activate autophagy and autophagy restricts pathogens such as Haemophilus parasuis through specific mechanisms. Autophagy is associated with the pathogenesis of H. parasuis. However, the mechanisms have not been clarified. Here, we monitored autophagy processes using confocal microscopy, western blot, and transmission electron microscopy (TEM) and found that H. parasuis SH0165 (high-virulent strain) but not HN0001 (non-virulent strain) infection enhanced autophagy flux. The AMPK/mTOR autophagy pathway was required for autophagy initiation and ATG5, Beclin-1, ATG7, and ATG16L1 emerged as important components in the generation of the autophagosome during H. parasuis infection. Moreover, autophagy induced by H. parasuis SH0165 turned to fight against invaded bacteria and inhibit inflammation. Then we further demonstrated that autophagy blocked the production of the cytokines IL-8, CCL4, and CCL5 induced by SH0165 infection through the inhibition of NF-κB, p38, and JNK MAPK signaling pathway. Therefore, our findings suggest that autophagy may act as a cellular defense mechanism in response to H. parasuis and provide a new way that autophagy protects the host against H. parasuis infection.

Published
2019
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2. Autophagy is a defense mechanism controlling Streptococcus suis serotype 2 infection in murine microglia cells

Author

Jinquan Li, Peng Xiang, Hui Jin, Lang Xu, Yan Zeng, Si Ming Zhang, Chaoxiong Yue, Hongde Xiao, Deshi Shi, Wei Zhou, Chenlu Hu, and Yushan Chen

Subjects
Autophagosome, Streptococcus suis, ATG5, Inflammation, Biology, Microbiology, Cell Line, Meningitis, Bacterial, ATG12, Hemolysin Proteins, Mice, 03 medical and health sciences, Streptococcal Infections, Autophagy, medicine, Animals, 030304 developmental biology, 0303 health sciences, Streptococcus suis serotype 2, General Veterinary, Microglia, 030306 microbiology, General Medicine, biology.organism_classification, medicine.anatomical_structure, Astrocytes, medicine.symptom
Abstract

Streptococcus suis (S. suis) is an important swine and human pathogen, causing severe meningitis with high morbidity and mortality worldwide. Microglial activation and inflammation are responsible for bacterial meningitis. S. suis has been identified to activate microglia, but the role of autophagy following S. suis infection in microglial cells remains elusive. In this study, using western blot, immunofluorescent staining and transmission electron microscopy (TEM), we demonstrated that S. suis serotype 2 (SS2) triggered autophagosome and enhanced autophagic flux in BV2 microglial cells. Autophagy activators, rapamycin, could further promote autophagy in S. suis-infected BV2 cells. Conversely, autophagy inhibitors including siRNA targeting ATG5, Beclin-1, ATG9a and ATG12 attenuated the autophagic process. Consistent with the in vitro results, autophagy was activated following S. suis infection in brain tissue including frontal cortex and hippocampus in a mouse model of meningitis. Further experiment showed that autophagy serves as a cellular defense mechanism to limit invaded bacteria and microglia inflammation in S. suis-infected BV2 cells. This is the first study reporting that the interaction between autophagy and microglia cells in response to S. suis infection. The possible mechanism involved could additionally suggest potential therapeutic approaches for bacterial meningitis.

Published
2021

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