Coinfection with Listeria monocytogenes potentlxtes the response of BALB/c mice against Leishmania major.

Protection against L. major is dependent on the stimulation of an anti-leishmanial T helper1 (Th1) response and the production of Interferon (IFN)-y. BALB/c mice develop a Th2 response and fatal infection with Leishmania major. Strategies that boost IL-12 production have shown to be protective. The innate response to Listeria monocytogenes is associated with IL-12 production. The co-infection of BALB/c mice with L. monocytogenes attenuates the course of L. major infection. Lesion sizes were smaller, and co-infected mice out-survived controls injected with L. major alone. The parasite load was reduced at site of injection, in draining lymph nodes (LN) and spleen. During the first week of infection, in-vitro Leishmania-restimulated LN cells from co-infected mice produced higher levels of IFN-7 and undetectable levels of IL-4 compared to controls. Significant IL-4 mRNA expression was detected in LN cells of control but not in co-infected mice.