Using mice deficient in the expression of NK-1R or the prophylactic administration of the NK-1R antagonist L703,606, we have demonstrated that substance P interactions with NK-1R are required for the increases in blood-brain barrier permeability, astrogliosis, increased CNS cellularity, and elevated numbers of microglia/macrophages associated with infection with the clinically relevant bacterial CNS pathogens Streptococcus pneumoniae, Neisseria meningitidis and Borrelia burgdorferi (Chauhan et al., 2008, 2011). This evidence concerns the gene TACR1 and infection.