Topological Aspects of the Blood–Brain and Blood–Cerebrospinal Fluid Barriers and Their Relevance in Inflammation

Abstract

In both multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis, the blood–brain barrier (BBB) is known to be compromised at the level of postcapillary venules. In addition to this segment of blood circulation, recent research has focused on the role of the choroid plexus (CP), which is crossed by encephalitogenic T-cells to enter the cerebrospinal fluid (CSF) and to reach the subarachnoid space (SAS). Here, cytokines can activate local antigen-presenting cells to enhance the transmission of inflammatory cells from the subpial vasculature into the SAS to evoke meningitis- and encephalitis-related diseases. However, overcoming the endothelium in the postcapillary venules and the epithelium in the CP do not seem to be the only mechanisms in the induction process of inflammation. Rather, as there is continuity between the stroma of the CP and the SAS, this continuity could serve as a direct pathway for inflammatory cells. In this review, we describe the morphological properties of barrier-related cells in both the brain vasculature and the CP to draw attention to possible mechanisms of the processes of inflammation in the central nervous system. We focus on permeability-related structures, such as tight junctions in endothelial cells of the BBB and in endothelial and epithelial cells of the CP, which represent the main site of the blood–CSF barrier proper.