Characteristics and mechanism of cerebral inflammatory response induced by Streptococcus parasuis clinical strains in mice

  Objective  To understand the characteristics and mechanism of the cerebral inflammatory response induced by Streptococcus parasuis clinical strains in mice.

  Methods  The bacterial loads, kinetics of inducible nitric oxide synthase (iNOS), pro-inflammatory cytokine IL-1β and NOD-like receptor (NOD1/2) transcription level in the brain of mice infected with clinical S. parasuis strain NN1, S. parasuis clinical strain BS26 and highly pathogenic S. suis strain P1/7 were analyzed with quantitative polymerase chain raction. The NO concentration, IL-1β and NOD1/2 mRNA transcription levels of the murine primary astrocyte and microglia cell line BV2 cell infected with aforementioned three strains were also evaluated.

  Results  S. parasuis clinical strains NN1 and BS26 persisted in the brain of infected mice for more than 48 hours. They could upregulate the transcription level of iNOS, IL-1β and NOD1/2 mRNA in the brain of infected mice at the early phase of infection. Microglia cells might play a more important role to induce the production of NO and IL-1β in the brains of mice infected with S. parasuis clinical strains NN1 and BS26. NOD1/2 receptors were crucial for the activation of astrocytes by S. parasuis clinical strains NN1 and BS26.

  Conclusion  S. parasuis clinical strains NN1 and BS26 could induce the cerebral inflammatory responses at the very early phase of infection via NOD1/2 receptors. Astrocytes and microglia played an important role in the cerebral inflammatory response induced by the infection of S. parasuis clinical strains on mice. In addition, the mechanism to activate astrocyte and microglia cells by the infection of S. parasuis clinical strains varied.