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Abstract

It has been reported that acute morphine administration modulates innate immune response to herpes simplex virus 1 (HSV-1) infection. In this study, the effect of acute morphine on innate resistance and its probable mechanisms in increasing the mortality rate during HSV-1 infection were investigated. Mice were infected with HSV-1 24 h prior to different doses of morphine or saline administration and the mortality rate was recorded. Spleen cells were obtained from morphine- or saline-treated mice, then natural killer (NK) cell activity and interferon-gamma (IFN-gamma) production were evaluated. The effect of morphine on white blood cells' capacity to induce protection against HSV-1 infection was evaluated by adoptive transfer of spleen cells to cyclophosphamide-treated mice that were previously infected with HSV-1. Furthermore, in a separate experiment, a different group of mice received corticosterone 24 h after HSV-1 infection. Mortality rate in high-dose acute morphine-treated mice increased significantly compared to saline-treated mice (p = 0.035). NK cell cytotoxicity and IFN-gamma mRNA levels also showed a significant reduction compared to those of control groups (p < 0.001 and p = 0.014, respectively). Corticosterone administration reduces innate resistance against HSV-1 infection compared to saline-treated mice (p = 0.044). Furthermore, adoptive transfer of normal but not morphine-treated spleen cells induces resistance against HSV infection in cyclophosphamide-injected mice (p = 0.009). The current study shows that acute morphine administration reduces white blood cells' capability to induce protection against HSV-1 infection via suppression of IFN-gamma production and NK cells activity. This may be due to the increase in corticosteroids. Further studies are needed to test the effect of acute morphine on other immune cells. Copyright 2007 S. Karger AG, Basel.

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Opioids, opioid receptors, and the immune response.

Lois McCarthy, Michele Wetzel, Judith Sliker … (2001)

It is now clear that opioid receptors participate in the function of the cells of the immune system, and evidence suggests that opioids modulate both innate and acquired immune responses. We review literature here which establishes that mu-, kappa-, and delta-opioid compounds alter resistance to a variety of infectious agents, including the Human Immunodeficiency Virus (HIV). The nature of the immunomodulatory activity of the opioids has been the subject of a great deal of research over the last ten years. There is increasing evidence that effects of opioids on the immune response are mediated at several levels. Modulation of the inflammatory response appears to be a target of these compounds, including effects on phagocytic activity, as well as the response of cells to various chemoattractant molecules. Moreover, findings from several laboratories have demonstrated the impact of opioid treatment on antibody responses, and the molecular basis for this effect is likely due, at least in part, to the modulation of both cytokine and cytokine receptor expression. Future research should provide a clearer understanding of the cellular and molecular targets of opioid action within the immune system.