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

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.