TAC1 and infection: 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).