Cyclosporin A treatment converts Leishmania donovani-infected C57BL/10 (curing) mice to a noncuring phenotype

Abstract

Cyclosporin A prevents visceralization of Leishmania major infection of BALB/c mice (N.C. Behforouz, C.D. Wenger, and B.A. Mathison, J. Immunol. 136:3067-3075, 1986; W. Solbach, K. Forberg, E. Kammerer, C. Bogdan, and M. Rollinghoff, J. Immunol. 134:702-707, 1986). We report that cyclosporin A exacerbates disseminated leishmaniasis caused by L. donovani in C57BL/10 mice. Normal mice challenged with 5 x 106 amastigotes intravenously cleared the infection within several months by spontaneous acquisition of cell-mediated immunity. In contrast, cyclosporin A administered daily intraperitoneally at a dose of 1.25 mg per mouse prevented development of curative immunity and converted C57BL/10 (curing) mice to a noncuring phenotype. A rationale for the contrasting effects of cyclosporin A in the two murine models of leishmaniasis is provided.