Activation of each subtype of TLR depends on specific circumstances, such as, TLR2-mediated neuroinflammation led to increased permeability in the BBB, promoting bacterial clearance in mice during meningitis; the absence of TLR2 led to the disruption in the conventional (TLR2-TNF-α) inflammatory response, and ultimately caused detrimental effects to the CNS [48]. This evidence concerns the gene TLR2 and infectious meningitis.