Abstract
Infection with certain bacteria, parasites, and viruses alters the host immune system to Leishmania major influencing disease outcome. Here, we determined the outcome of a chronic infection with Trypanosoma brucei brucei on cutaneous leishmaniasis (CL) caused by L. major. C57BL/6 mice infected with T. b. brucei were given a sub-curative treatment with diminazene aceturate then coinfected with L. major by vector bites. Our results revealed that infection with T. b. brucei controls CL pathology. Compared to controls, coinfected mice showed a significant decrease in lesion size (P < 0.05) up to 6 weeks post-infection and a significant decrease in parasite burden (P < 0.0001) at 3 weeks post-infection. Protection against L. major resulted from a non-specific activation of T cells by trypanosomes. This induced a strong immune response characterized by IFN-γ production at the site of bites and systemically, creating a hostile inflammatory environment for L. major parasites and conferring protection from CL.
Highlights
Cutaneous leishmaniasis (CL) is an infectious disease caused by Leishmania parasites
We show that T. b. brucei parasites create a nonspecific intense pro-inflammatory response, local, and systemic, characterized by high levels of IFN-γ that creates an adverse environment for Leishmania parasites
Mice coinfected with T. b. brucei and L. major exhibited a lower rate of weight gain beyond the second week after L. major transmission compared to animals infected with L. major alone (Supplementary Figure 1)
Summary
Cutaneous leishmaniasis (CL) is an infectious disease caused by Leishmania parasites. CL affects man and other mammals, causing ulcers in the skin and mucous membranes. Leishmania parasites are transmitted by the bite of vector sand flies together with vector-derived factors as part of a virulent infectious inoculum [2,3,4]. Protective adaptive immunity to CL depends on the induction of specific Th1-polarized CD4+T cells that produce pro-inflammatory cytokines such as IL-12, IFN-γ, and TNF-α, responsible for macrophage activation and parasite killing [5]. A Th-2 polarized immune response with T cells producing cytokines such as IL-13, IL-4, IL-10, and IL-5 are associated to susceptibility to Leishmania and an increase in the size and severity of L. major lesions [5]
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