Abstract
A nontoxic dose of Sambucol, an immunomodulator commercially sold as an immune stimulator,
was examined in murine models of leishmaniasis and malaria. Sambucol causes a shift
in the immune response, as demonstrated in human monocyte cultures, to Th1 (inflammation-associated)
responses. Treatment of leishmania-infected mice with Sambucol delayed the development
of the disease. As there was no direct in vitro anti-leishmanial effect, the observed partial protection in vivo is most likely related to immune modulation. Although increased Th1 responses are
associated with protection from leishmaniasis, they are considered to be the main
immunopathological processes leading to cerebral malaria. Administration of Sambucol
to mice prior to and following infection with Plasmodium berghei ANKA increased the incidence of cerebral malaria, while administration of Sambucol
after infection had no effect on the disease. The results demonstrate how an inflammatory-like
response may alleviate or exacerbate clinical symptoms of disease and hint at the
importance of administration timing. The overall effect of immunomodulator administration
depends on the ongoing immune response and the Th1/Th2 balance determined by both
host and parasite defense mechanisms.
Key words
malaria - leishmaniasis - Sambucol -
Sambucus nigra L. (Sambucaceae) - immunomodulation - cytokines
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golenser@md.huji.ac.il
