PMID- 30117097
OWN - NLM
STAT- MEDLINE
DCOM- 20181105
LR  - 20181114
IS  - 1573-6830 (Electronic)
IS  - 0272-4340 (Linking)
VI  - 38
IP  - 7
DP  - 2018 Oct
TI  - Mechanisms of Blood Brain Barrier Disruption by Different Types of Bacteria, and 
      Bacterial-Host Interactions Facilitate the Bacterial Pathogen Invading the Brain.
PG  - 1349-1368
LID - 10.1007/s10571-018-0609-2 [doi]
AB  - 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-kappaB 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-1alpha, IL-1beta, IL-6, TNF-alpha, MCP-1, 
      macrophage inflammatory proteins-1 alpha (MIP1alpha) 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 to target the common carboxy-terminal domain of LR to start initial 
      interaction with brain endothelium, then invade the brain. H. influenza type b 
      (HiB), can induce BBB permeability through TJ disruption. LR and PAFR binding 
      sites have been recognized as common routes of CNS entrance by Neisseria 
      meningitidis. N. meningitidis species also initiate binding to BMECs and induces 
      AJs deformation, as well as inducing specific cleavage of the TJ component 
      occludin through the release of host MMP-8. Escherichia coli bind to BMECs 
      through LR, resulting in IL-6 and IL-8 release and iNOS production, as well as 
      resulting in disassembly of TJs between endothelial cells, facilitating BBB 
      disruption. Therefore, obtaining knowledge of BBB disruption by different types 
      of bacterial species will provide a picture of how the bacteria enter the central 
      nervous system (CNS) which might support the discovery of therapeutic strategies 
      for each bacteria to control and manage infection.
FAU - Al-Obaidi, Mazen M Jamil
AU  - Al-Obaidi MMJ
AD  - Department of Biomedical Science, Faculty of Medicine and Health Sciences, 
      Universiti Putra Malaysia, 43400 UPM, Serdang, Selangor, Malaysia. 
      mazen_m@upm.edu.my.
FAU - Desa, Mohd Nasir Mohd
AU  - Desa MNM
AUID- ORCID: 0000-0003-0200-4796
AD  - Department of Biomedical Science, Faculty of Medicine and Health Sciences, 
      Universiti Putra Malaysia, 43400 UPM, Serdang, Selangor, Malaysia. 
      mnasir@upm.edu.my.
AD  - Halal Products Research Institute, Universiti Putra Malaysia, Serdang, Selangor, 
      Malaysia. mnasir@upm.edu.my.
LA  - eng
GR  - 5524924/fundamental research grant scheme/
GR  - 5526406/long term research grant scheme/
PT  - Journal Article
PT  - Review
DEP - 20180816
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
SB  - IM
MH  - Animals
MH  - Bacteria/growth & development/*metabolism/pathogenicity
MH  - Blood-Brain Barrier/*metabolism/*microbiology
MH  - Brain/*metabolism/*microbiology
MH  - Capillary Permeability/*physiology
MH  - Endothelium, Vascular/metabolism/microbiology
MH  - Host-Parasite Interactions/physiology
MH  - Humans
OTO - NOTNLM
OT  - Bacterial infection
OT  - Blood brain barrier
OT  - Meningitis
OT  - Therapeutic strategies
EDAT- 2018/08/18 06:00
MHDA- 2018/11/06 06:00
CRDT- 2018/08/18 06:00
PHST- 2018/03/20 00:00 [received]
PHST- 2018/08/06 00:00 [accepted]
PHST- 2018/08/18 06:00 [pubmed]
PHST- 2018/11/06 06:00 [medline]
PHST- 2018/08/18 06:00 [entrez]
AID - 10.1007/s10571-018-0609-2 [pii]
AID - 10.1007/s10571-018-0609-2 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2018 Oct;38(7):1349-1368. doi: 10.1007/s10571-018-0609-2. 
      Epub 2018 Aug 16.