Complement C1q and C3 Are Critical for the Innate Immune Response to Streptococcus pneumoniae in the Central Nervous System

摘要: Previous studies suggest that the complement system can contribute to limiting pneumococcal outgrowth within CNS. In this study, we evaluated role of in activation innate immune response and development prognosis-relevant intracranial complications a murine model meningitis. Thereby, used mice deficient C1q, lacking only classical pathway, C3, all three pathways. At 24 h after intracisternal infection, bacterial titers CNS were almost 12- 20-fold higher C1q- C3-deficient-mice, respectively, than wild-type mice. Mean CSF leukocyte counts reduced by 47 73% respectively. Intrathecal reconstitution with serum C3-deficient restored both ability combat infection leukocytes egress into CSF. The altered recruitment was paralleled strong reduction brain expression cytokines chemokines. dampened accompanied meningitis-induced complications, but, surprisingly, also worsening short-term outcome. latter seems be due more severe bacteremia (12- 120-fold respectively) and, consecutively, systemic complications. Thus, our study demonstrated for first time plays an integral mounting intense host Streptococcus pneumoniae