Mechanisms of Blood Brain Barrier Disruption by Different Types of Bacteria, and Bacterial–Host Interactions Facilitate the Bacterial Pathogen Invading the Brain

• Published in: Cellular and molecular neurobiology 2018-10, Vol.38 (7), p.1349-1368
• Main Authors: Al-Obaidi, Mazen M. Jamil, Desa, Mohd Nasir Mohd
• Format: Article
• Language: English
• Subjects: Adherens junctions; Animals; Bacteria; Bacteria - growth & development; Bacteria - metabolism; Bacteria - pathogenicity; Biomedical and Life Sciences; Biomedicine; Blood-brain barrier; Blood-Brain Barrier - metabolism; Blood-Brain Barrier - microbiology; Brain - metabolism; Brain - microbiology; Capillary Permeability - physiology; CD31 antigen; Cell adhesion & migration; Cell adhesion molecules; Cell Biology; Central nervous system; Choline; E-cadherin; E-selectin; Endothelial cells; Endothelium; Endothelium, Vascular - metabolism; Endothelium, Vascular - microbiology; Gram-negative bacteria; Host-Parasite Interactions - physiology; Humans; Inflammation; Influenza; Intercellular adhesion molecule 1; Interleukin 6; Interleukin 8; Laminin; Listeria monocytogenes; Macrophages; Membrane permeability; Mesenchyme; Monocyte chemoattractant protein 1; Monocytes; Neurobiology; Neurosciences; Nitric oxide; Pathogens; Permeability; Proteins; Review Paper; Species; Streptococcus infections; Streptococcus pneumoniae; Tight junctions
• ISSN: 0272-4340; 1573-6830; 1573-6830
• DOI: 10.1007/s10571-018-0609-2

This review aims to elucidate the different mechanisms of blood brain barrier (BBB) disruption that may occur due to invasion by different types of bacteria, as well as to show the bacteria–host interactions that assist the bacterial pathogen in invading the brain. For example, platelet-activating factor receptor (PAFR) is responsible for brain invasion during the adhesion of pneumococci to brain endothelial cells, which might lead to brain invasion. Additionally, the major adhesin of the pneumococcal pilus-1, RrgA is able to bind the BBB endothelial receptors: polymeric immunoglobulin receptor (pIgR) and platelet endothelial cell adhesion molecule (PECAM-1), thus leading to invasion of the brain. Moreover, Streptococcus pneumoniae choline binding protein A (CbpA) targets the common carboxy-terminal domain of the laminin receptor (LR) establishing initial contact with brain endothelium that might result in BBB invasion. Furthermore, BBB disruption may occur by S. pneumoniae penetration through increasing in pro-inflammatory markers and endothelial permeability. In contrast, adhesion, invasion, and translocation through or between endothelial cells can be done by S. pneumoniae without any disruption to the vascular endothelium, upon BBB penetration. Internalins (InlA and InlB) of Listeria monocytogenes interact with its cellular receptors E-cadherin and mesenchymal-epithelial transition (MET) to facilitate invading the brain. L. monocytogenes species activate NF-κB in endothelial cells, encouraging the expression of P- and E-selectin, intercellular adhesion molecule 1 (ICAM-1), and Vascular cell adhesion protein 1 (VCAM-1), as well as IL-6 and IL-8 and monocyte chemoattractant protein-1 (MCP-1), all these markers assist in BBB disruption. Bacillus anthracis species interrupt both adherens junctions (AJs) and tight junctions (TJs), leading to BBB disruption. Brain microvascular endothelial cells (BMECs) permeability and BBB disruption are induced via interendothelial junction proteins reduction as well as up-regulation of IL-1α, IL-1β, IL-6, TNF-α, MCP-1, macrophage inflammatory proteins-1 alpha (MIP1α) markers in Staphylococcus aureus species. Streptococcus agalactiae or Group B Streptococcus toxins (GBS) enhance IL-8 and ICAM-1 as well as nitric oxide (NO) production from endothelial cells via the expression of inducible nitric oxide synthase (iNOS) enhancement, resulting in BBB disruption. While Gram-negative bacteria, Haemophilus influenza OmpP2 is able