A systemic mechanism of increased transendothelial migration of leukocytes through the blood-brain barrier in hepatic encephalopathy
Abstract
Background: Hepatic encephalopathy (HE) is a frequent neurological complication of cirrhosis. Evidence suggests a synergic pathophysiological implication of hyperammonemia and systemic inflammation. In addition, the blood-brain barrier (BBB) permeability can be impaired in cirrhotic patients, notably in those displaying HE. We hypothesized that systemic inflammation could trigger leukocytes transendothelial migration (TEM) through the BBB in cirrhotic patients and especially those with HE.
Keywords
junctional adhesion molecules
MMP
matrix metalloproteinase
MELD
model for end-stage liver disease
GGT
gamma-glutamine transferase
AST
aspartate amino transferase
ALT
alanine amino transferase
PT
prothrombin time
CRP
C-reactive protein
PCT
procalcitonin
PS-100Beta
Transendothelial migration Leukocytes Cirrhosis Hepatic encephalopathy Abbreviations: HE
hepatic encephalopathy BBB
blood brain barrier TEM
transendothelial migration EC
endothelial cells JAMs
junctional adhesion molecules MMP
matrix metalloproteinase MELD
model for end-stage liver disease GGT
gamma-glutamine transferase AST
aspartate amino transferase ALT
alanine amino transferase PT
prothrombin time CRP
C-reactive protein PCT
procalcitonin PS-100Beta
protein S-100 Beta
Transendothelial migration
Leukocytes
Cirrhosis
Hepatic encephalopathy
Abbreviations: HE
hepatic encephalopathy
BBB
blood brain barrier
TEM
transendothelial migration
EC
endothelial cells
JAMs
Domains
Life Sciences [q-bio]| Origin | Files produced by the author(s) |
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