The effects of an immunopotentiating
drug Inosine Pranobex (
isoprinosine) were investigated in an experimental
cutaneous leishmaniasis model. The highly susceptible BALB/c mice treated orally with
isoprinosine developed significantly delayed onset of disease when infected with Leishmania major compared to untreated mice. The
drug itself is not toxic to the parasite up to millimolar levels in vitro. The increase in resistance to L. major
infection is accompanied by a marked decrease in the CD4+/CD8+ ratio and the leishmanial
antigen-specific proliferative response of the spleen cells of
isoprinosine-treated mice compared to untreated mice. There was a significant increase in the production of IFN-gamma but a decrease in the secretion of
IL-3 and
IL-4 by the spleen cells of
isoprinosine-treated mice in response to
concanavalin A with or without L. major
infection compared to untreated controls. There was, however, no significant difference in the level of
IL-2 production by the spleen cells between mice with or without
isoprinosine treatment. These data are consistent with the interpretation that
isoprinosine potentiates the resistance to leishmanial
infection by up-regulating the host-protective Th1 cells and down-regulating the disease-promoting Th2 cells or, alternatively, by increasing CD8+ T-cell function.