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Updated: Nov 5, 2025

Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
Published on: February 9, 2014
Autophagy is a defense mechanism controlling Streptococcus suis serotype 2 infection in murine microglia cells
Chaoxiong Yue1, Chenlu Hu1, Peng Xiang1
1Brain Science and Advanced Technology Institute, Wuhan University of Science and Technology, Wuhan, China; Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology, Wuhan, China.
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.
Insights
Streptococcus suis (S. suis) infection activates autophagy in microglial cells, acting as a defense mechanism against bacterial meningitis. This study reveals autophagy
Area of Science:
- Neuroscience
- Immunology
- Microbiology
Background:
- Streptococcus suis (S. suis) causes severe bacterial meningitis in humans and swine.
- Microglial activation and inflammation are key pathological features of S. suis meningitis.
- The role of autophagy in microglial response to S. suis infection was previously unknown.
Purpose of the Study:
- To investigate the role of autophagy in microglial cells during S. suis infection.
- To determine if autophagy acts as a defense mechanism against S. suis in microglia.
Main Methods:
- Utilized western blot, immunofluorescent staining, and transmission electron microscopy (TEM) in BV2 microglial cells.
- Employed autophagy activators (rapamycin) and inhibitors (siRNA targeting ATG5, Beclin-1, ATG9a, ATG12).
- Analyzed autophagy activation in brain tissues from a mouse model of S. suis meningitis.
Main Results:
- S. suis serotype 2 (SS2) infection triggered autophagosome formation and enhanced autophagic flux in BV2 microglial cells.
- Autophagy activators increased autophagy, while inhibitors attenuated it in S. suis-infected cells.
- Autophagy was activated in brain tissues (frontal cortex, hippocampus) of infected mice.
Conclusions:
- Autophagy is activated in microglial cells in response to S. suis infection.
- Autophagy functions as a cellular defense mechanism to limit S. suis invasion and microglial inflammation.
- This interaction highlights potential therapeutic strategies for bacterial meningitis.
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