As the organ of highest metabolic demand, utilizing over 25% of total body glucose utilization via an enormous vasculature with one capillary every 73 μm, the brain evolves a barrier at the capillary and postcapillary venules to prevent toxicity during serum fluctuations in metabolites and hormones, to limit brain swelling during inflammation, and to prevent pathogen invasion. Understanding of neuroprotective barriers has since evolved to incorporate the neurovascular unit (NVU), the blood-cerebrospinal fluid (CSF) barrier, and the presence of CNS lymphatics that allow leukocyte egress. Identification of the cellular and molecular participants in BBB function at the NVU has allowed detailed analyses of mechanisms that contribute to BBB dysfunction in various disease states, which include both autoimmune and infectious etiologies. This chapter will introduce some of the cellular and molecular components that promote barrier function but may be manipulated by inflammatory mediators or pathogens during neuroinflammation or neuroinfectious diseases.

Original languageEnglish
Title of host publicationContemporary Clinical Neuroscience
PublisherSpringer Nature
Number of pages40
StatePublished - 2019

Publication series

NameContemporary Clinical Neuroscience
ISSN (Print)2627-535X
ISSN (Electronic)2627-5341


  • Blood-brain barrier
  • Central nervous system
  • Innate immunity
  • Neuroinfectious diseases
  • Tight junctions


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