TY  - JOUR
ID  - discovery2921
AV  - public
SP  - 419 
Y1  - 2004///
IS  - 6
TI  - Electric foot-shock stress drives TNF-alpha production in the liver of IL-6-deficient mice
A1  - Chida, Y
A1  - Sudo, N
A1  - Motomura, Y
A1  - Kubo, C
EP  -  424
VL  - 11
UR  - https://discovery.ucl.ac.uk/id/eprint/2921/
JF  - NEUROIMMUNOMODULAT
PB  - KARGER
KW  - anti-inflammatory effect
KW  -  apoptosis
KW  -  electric foot-shock
KW  -  IL-6
KW  -  liver injury
KW  -  psychoneuroimmunology
KW  -  psychophysical stress
KW  -  TNF-alpha
KW  -  PLASMA INTERLEUKIN-6
KW  -  IMMOBILIZATION STRESS
KW  -  IL-6
KW  -  CELLS
KW  -  RATS
KW  -  EXPRESSION
KW  -  INDUCTION
KW  -  INJECTION
KW  -  ENDOTOXIN
KW  -  PATHWAYS
N2  - Objectives: Accumulating evidence has shown that interleukin-6 (IL-6) has pleiotropic effects on a variety of biological functions, including its antiapoptotic potential during liver injury. Our previous work demonstrated that restraint stress-induced elevation of plasma IL-6 negatively regulates plasma tumor necrosis factor-alpha (TNF-alpha). Herein, we further clarified the mechanism underlying the above finding and investigated the effect of IL-6 on liver apoptosis triggered by stress. Methods: Male C57BL/6J and IL-6-deficient C57BL/SV129 mice were exposed to 1 h of electric foot-shock stress. Thereafter, the serum, liver and spleen TNF-alpha levels were measured at several time points. Serum alanine aminotransferase (ALT), liver caspase-3 and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling ( TUNEL) activities were analyzed to evaluate the severity of liver injury and apoptosis. Results: The liver, but not the spleen, of the IL-6-deficient mice exhibited a significant increase in TNF-alpha level after stress in parallel with serum TNF-alpha elevation, whereas no such TNF-alpha responses were found in the wild animals. No significant differences in stress-induced elevation of serum ALT levels, liver caspase-3 activities and the number of TUNEL-positive hepatocytes were found between the wild and IL-6-deficient mice. Conclusions: Taken together, these results indicate that IL-6 may play a critical role in suppressing TNF-alpha production in the liver, thereby decreasing the blood TNF-alpha level. In contrast, IL-6 secretion was shown to have no protective effect on stress-triggered liver injury. Copyright (C) 2004 S. Karger AG, Basel.
SN  - 1021-7401
ER  -