Mounting evidence has shown that the development and progression of pneumococcal meningitis and its intracranial complications are not only due to an uncontrolled bacterial growth in the central nervous system (CNS), but also dependent largely on the host innate immunity-initiated inflammatory response through the recognition of pathogen-associated molecular patterns (PAMPs) on the invaded microbial pathogens by the pattern recognition receptors (PRRs) such as toll-like receptor 2 (TLR2) and its adaptor protein myeloid differentiation factor 88 (MyD88) [10–12]. Here, TLR2 is linked to pneumococcal meningitis.