Abstract
The choroid plexus (CP) forming the blood–cerebrospinal fluid (B-CSF) barrier is among the least studied structures of the central nervous system (CNS) despite its clinical importance. The CP is an epithelio-endothelial convolute comprising a highly vascularized stroma with fenestrated capillaries and a continuous lining of epithelial cells joined by apical tight junctions (TJs) that are crucial in forming the B-CSF barrier. Integrity of the CP is critical for maintaining brain homeostasis and B-CSF barrier permeability. Recent experimental and clinical research has uncovered the significance of the CP in the pathophysiology of various diseases affecting the CNS. The CP is involved in penetration of various pathogens into the CNS, as well as the development of neurodegenerative (e.g., Alzheimer´s disease) and autoimmune diseases (e.g., multiple sclerosis). Moreover, the CP was shown to be important for restoring brain homeostasis following stroke and trauma. In addition, new diagnostic methods and treatment of CP papilloma and carcinoma have recently been developed. This review describes and summarizes the current state of knowledge with regard to the roles of the CP and B-CSF barrier in the pathophysiology of various types of CNS diseases and sets up the foundation for further avenues of research.
Highlights
The central nervous system (CNS) is protected against harmful substances contained in the blood by the blood– brain barrier (BBB) and the blood–cerebrospinal (B-cerebrospinal fluid (CSF)) barrier [1–3]
Concluding remarks As we have described in this review, the pathogenesis and pathophysiology of various diseases is more or less linked with improper functioning of the choroid plexus (CP) and blood–cerebrospinal fluid (B-CSF) barrier
We may conclude that the major changes are in the production of different proteins by CP epithelial cells, expression of tight junctions (TJs) and transporter proteins as well as immune cell trafficking
Summary
The central nervous system (CNS) is protected against harmful substances contained in the blood by the blood– brain barrier (BBB) and the blood–cerebrospinal (B-CSF) barrier [1–3]. Intensified cell death in the CP could lead to alteration in the B-CSF barrier function and facilitate penetration of bacteria and leukocytes into the CSF of the ventricular system reaching up to the brain parenchyma [132] Another mechanism by which Streptococcus suis may enter the CSF involves invasion from the basolateral side of CP epithelial cells, transport within endocytic vacuoles to the apical side and exocytosis on the apical membrane. No Streptococcus pneumoniae was detected in the early stage of infection, while at 8 and 14 h after infection the bacteria were found associated with CP vessels This may be caused by increased basal levels of platelet-activating factor (PAF), Fig. 3 Schematic illustration showing the various invasion strategies of different pathogens (bacteria, viruses and parasites) through the B-CSF barrier into the CNS. Concurrent inhibition of MAPK signaling pathways potentially reduces infection [142]
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