Coinfection With Trypanosoma brucei Confers Protection Against Cutaneous Leishmaniasis

Frontiers in Immunology

Stefan Magez¹  Ian N. Moore²  Claudia I. Brodskyn³  Fabiano Oliveira⁵  Shannon Townsend⁵  Lais Pereira⁵  Jesus G. Valenzuela⁵  Shaden Kamhawi⁵  Sonia Metangmo⁵  Claudio Meneses⁵ 

[1] Ghent University Global Campus, Incheon, South Korea;Infectious Disease Pathogenesis Section, Comparative Medicine Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, United States;Laboratorio da interação parasita hospedeito e epidemiologia, Instituto de Pesquisas Gonçalo Moniz, FIOCRUZ, Salvador, Brazil;Laboratory for Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium;Vector Molecular Biology Section, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, United States;

关键词: Leishmania major;    Trypanosoma brucei;    coinfection;    inflammation;    cellular immunity;    humoral immunity;   

DOI  :  10.3389/fimmu.2018.02855

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown