Loss of Morphine-induced Suppression of NK Cell activity and T-cell Functions in µ-Opioid Receptor Knockout Mice
Richard J. Weber, Ricardo Gomez-Flores, Ichiro Sora and George R. Uhl
DOI : 10.3844/ajisp.2006.35.39
American Journal of Immunology
Volume 2, 2006
In vivo administration of µ-opioid receptor selective agonists to various species is known to suppress lymphocyte, NK cell, and macrophage functions, in addition to mediate pain relief and euphoria. Using a mouse model in which the µ-opioid receptor gene was disrupted by targeted homologous recombination, we explored the involvement of this receptor in natural killer (NK) cell activity and T lymphocyte function. Following peripheral morphine administration, NK cell activity was not affected in homozygous µ-opioid receptor knockout mice, heterozygous animals marginally responded to the immunosuppressive effects of the drug, while wild-type animals were significantly suppressed. In addition, splenic T-cell proliferative responses to concanavalin A, phytohemaglutinin and an antibody to T-cell receptorabαβ (TCR) plus interleukin-2 were not affected by morphine treatment in µ-opioid receptor knockout homozygous and heterozygous mice, whereas morphine significantly suppressed T-cell proliferation in wild-type mice. Taken together, these results suggest a role of the µ-opioid receptor in immunoregulation.
© 2006 Richard J. Weber, Ricardo Gomez-Flores, Ichiro Sora and George R. Uhl. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.