The effect of IL-13 on the course and outcome of infection with Leishmania major in BALB/c mice

Abstract

Leishmaniasis is a vector-borne disease caused by an intracellular protozoan parasite of the genus Leishmania. Female sandflies of the Phlebotominae subfamily carry the parasite,c and are primarily responsible for the transmission of this disease. BALB/c mice are known to be susceptible to Leishmania major, and thus injecting them with the parasite induces leishmaniasis. The disease provokes a Th2 immune response as IFN- levels decrease and IL-4 levels increase when mice are treated with the high dose form. However, when treated with the low dose form, the mice express high levels of IFN- and low levels of IL-4 thus acting as a resistant host, mediated by a Th1 response. Th1 cells are very important for the initiation of a cell-mediated immune response opposed to intracellular pathogens such as Leishmania major. On the other hand, Th2 are important for the induction of humoral immune responses since they secrete cytokines involved in the activation and differentiation of B cells into antibody- secreting plasma cells. In our project, it was of major interest to assess the role of IL-13 in shaping the course of infection if administered early in infection, especially in BALB/c mice infected with low dose of Leishmania major which are suspected to become resistant to the parasite. The addition of exogenous IL-13 showed suppression of IFN- levels and proved to affect the course of infection of leishmaniasis in a way that worsens the disease. In contrary to what was believed to be the case, our study gave further evidence that IL-4 was not the major affecter in the cytokine interplay during the inhibition of Th2/Th1 switch.