Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26041953
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Clin+Exp+Hepatol
2015 ; 5
(Suppl 1
): S21-8
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Neuroinflammation in hepatic encephalopathy: mechanistic aspects
#MMPMID26041953
Jayakumar AR
; Rama Rao KV
; Norenberg MD
J Clin Exp Hepatol
2015[Mar]; 5
(Suppl 1
): S21-8
PMID26041953
show ga
Hepatic encephalopathy (HE) is a major neurological complication of severe liver
disease that presents in acute and chronic forms. While elevated brain ammonia
level is known to be a major etiological factor in this disorder, recent studies
have shown a significant role of neuroinflammation in the pathogenesis of both
acute and chronic HE. This review summarizes the involvement of ammonia in the
activation of microglia, as well as the means by which ammonia triggers
inflammatory responses in these cells. Additionally, the role of ammonia in
stimulating inflammatory events in brain endothelial cells (ECs), likely through
the activation of the toll-like receptor-4 and the associated production of
cytokines, as well as the stimulation of various inflammatory factors in ECs and
in astrocytes, are discussed. This review also summarizes the inflammatory
mechanisms by which activation of ECs and microglia impact on astrocytes leading
to their dysfunction, ultimately contributing to astrocyte swelling/brain edema
in acute HE. The role of microglial activation and its contribution to the
progression of neurobehavioral abnormalities in chronic HE are also briefly
presented. We posit that a better understanding of the inflammatory events
associated with acute and chronic HE will uncover novel therapeutic targets
useful in the treatment of patients afflicted with HE.