Acute morphine administration reduces white blood cells' capability to induce innate resistance against HSV-1 infection in BALB/c mice

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. Methods: 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- � (IFN- � ) 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.
Results: Mortality rate in high-dose acute morphinetreated
mice increased significantly compared to salinetreated
mice (p = 0.035). NK cell cytotoxicity and IFN- � 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). Conclusions: The current study shows that acute
morphine administration reduces white blood cells’ capability
to induce protection against HSV-1 infection via suppression
of IFN- � 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