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Increased splenocyte proliferative response and cytokine production in beta-endorphin-deficient mice

MPS-Authors

Refojo,  D
Max Planck Institute of Psychiatry, Max Planck Society;

Kovalovsky,  D
Max Planck Institute of Psychiatry, Max Planck Society;

Young,  JI
Max Planck Institute of Psychiatry, Max Planck Society;

Rubinstein,  M
Max Planck Institute of Psychiatry, Max Planck Society;

Holsboer,  F
Max Planck Institute of Psychiatry, Max Planck Society;

Reul,  JMHM
Max Planck Institute of Psychiatry, Max Planck Society;

Low,  MJ
Max Planck Institute of Psychiatry, Max Planck Society;

Arzt,  E
Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Refojo, D., Kovalovsky, D., Young, J., Rubinstein, M., Holsboer, F., Reul, J., et al. (2002). Increased splenocyte proliferative response and cytokine production in beta-endorphin-deficient mice. Journal of Neuroimmunology, 131(1-2), 126-134.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000E-A145-6
Abstract
We used beta-endorphin-deficient mice as a novel approach to confirm the physiological role that opioid peptides play in the development or regulation of the immune system. We found that mice lacking beta-endorphin possessed an enhanced immune response, measured in terms of splenocyte proliferation and interleukin (IL)-2 mRNA levels, in vitro production of the splenic macrophage inflammatory cytokines IL-6 and Tumor Necrosis Factor (TNF)-alpha and plasma IL-6 following lipopolysaccharide (LPS) administration. beta-Endorphin- deficient mice had attenuated increases of plasma ACTH and corticosterone levels in response to LPS. These results are consistent with a postulated inhibitory role of endogenous beta-endorphin on the immune system at multiple levels. (C) 2002 Elsevier Science B.V. All rights reserve