TACR1 and bacterial infectious disease: Taken together, the robust constitutive and functional expression of the full-length NK-1R isoform by human microglia and astrocytes, and the ability of SP to augment inflammatory signaling pathways and mediator production by these cells, support the contention that SP/NK-1R interactions play a significant role in the damaging neuroinflammation and neurological sequelae associated with bacterial infections of the CNS in human subjects.