Kinetics of an experimental inflammatory reaction induced by Leishmania major during the implantation of paraffin tablets in mice

In leishmaniasis, macrophages play important but potentially divergent role s. They act as the host cell in which the parasite may reside and replicate , and, at the same time, they act as an effector cell with the potential to eliminate the parasite. In this work, we experimentally induced an inflamm atory model that provokes a continued recruitment of the monocytes to the s ite of inflammation. This model was carried out by means of im planting par affin tablets under the skin of Balb/c or C57BL/6 mice. Mice were then infe cted with Leishmania major to determine how the monocyte inflammatory respo nse to paraffin could influence the course of infection with L. major. Mice were sacrificed 15, 21, 30, and 45 days after infection, and skin and infl ammatory capsule were collected for histopathology. At 15 days and 21 days, the lesions induced by L. major in combination with paraffin contained mar kedly increased numbers of parasites relative to lesions in parallel contro l animals infected with L. major (without paraffin). Both Balb/c and C57BL/ 6 mice exhibited high parasite numbers in their lesions. The intense parasi te burden observed following paraffin implantation would suggest that the m onocytes-macrophages that are recruited to the lesion are acting more as a host cell permitting parasite growth than as an effector cell capable of el iminating L. major. At later times, the two strains of mice stratified acco rding to their genetic susceptibility/resistance profiles. Susceptible Balb /c mice continue to have large parasite burdens, whereas the resistant C56B L/6 mice begin to control parasite numbers. This later observation indicate s that the genetic difference between susceptible and resistant strains is not due to differences in monocyte recruitment and cannot be reversed throu gh the altering of monocyte inflammation.