A Possible Role for Prostaglandins in Regulation of Disease in Murine Cutaneous Leishmaniasis

Abstract

Following intradermal inoculation of Leishmania major promastigotes, various strains of inbred mice develop either of two distinct disease patterns. A majority of inbred strains develop small, ulcerating lesions at the cutaneous injection site. These lesions spontaneously resolve over a period of several weeks or months. In contrast, BALB/c mice develop severe local lesions, as well as multiple metastic lesions, with death the invariable outcome of infection.^1,2 Genetic susceptibility is controlled by cells of the hematopoietic system since lethally irradiated BALB/c mice, when reconstituted with bone marrow from genetically resistant B10.D2 mice, develop an infection pattern characteristic of the cell donor³, BALB/c mice can be altered to heal a infection by prior sublethal (550 rad) irradiation. Reconstitution of these mice with normal Lyl⁺ T cells reverses the prophylactic effect of irradiation. BALB/c mice treated in vivo with antibodies directed against the L3TA⁺ subset of T cells also heal infection. These, as well as other studies, suggest that Lyl⁺, L3TV cells play a central role in either the nonhealing or exacerbation of L. major infections in BALB/c mice.