Remarkably, blockage of NF-κB p65 and/or MAPK p38 with their specific inhibitors strongly attenuated B7-H3-amplified TNF-α, IL-1β, IL-6, and MCP-1 production in the brain of S. pneumoniae-infected mice, suggesting that B7-H3-induced additional activation of both NF-κB p65 and MAPK p38 is predominantly responsible for B7-H3-amplified inflammatory response during experimental pneumococcal meningitis. This evidence concerns the gene CCL2 and pneumococcal meningitis.