Concanavalin-A stimulates IL-17 and nitric oxide production and induces macrophage polarization and resistance to Trypanosoma cruzi infection.

Autor: Zanluqui NG; Instituto Carlos Chagas, Fiocruz-PR, Curitiba, Paraná, Brazil; Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná, Brazil., Lovo-Martins MI; Instituto Carlos Chagas, Fiocruz-PR, Curitiba, Paraná, Brazil; Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná, Brazil., Malvezi AD; Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná, Brazil., Panis C; Laboratório de Mediadores Inflamatórios, Universidade Estadual do Oeste do Paraná, Francisco Beltrão, PR, Brazil., da Silva RV; Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná, Brazil., Tatakihara VLH; Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná, Brazil., Felipe I; Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná, Brazil., Martins-Pinge MC; Departamento de Ciências Fisiológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil., Wowk PF; Instituto Carlos Chagas, Fiocruz-PR, Curitiba, Paraná, Brazil. Electronic address: pryscilla.wowk@fiocruz.br., Pinge-Filho P; Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná, Brazil. Electronic address: pingefilho@uel.br.
Jazyk: angličtina
Zdroj: Life sciences [Life Sci] 2020 Oct 01; Vol. 258, pp. 118137. Date of Electronic Publication: 2020 Jul 24.
DOI: 10.1016/j.lfs.2020.118137
Abstrakt: Aims: Chagas disease is a neglected tropical disease. The ability of Trypanosoma cruzi to survive within phagocytes is likely a critical factor for T. cruzi dissemination in the host. For control of the parasite load and host survival, macrophage action is required. Concanavalin-A (Con-A) presents properties that modulate immune functions and protect hosts from several experimental infectious diseases. Here, we evaluated the effects of Con-A on peritoneal macrophages as well as on the course of experimental infection by T. cruzi.
Main Methods: BALB/c mice, a susceptible model for T. cruzi infection, were treated with Con-A via the intraperitoneal route and 3 days later infected with T. cruzi. We quantified parasitemia, cytokines and nitric oxide (NO). Peritoneal exudate and macrophages were collected for macrophage phenotyping and cell viability, NO and cytokine detection, as well as for T. cruzi internalization and release index determination.
Key Findings: Con-A treatment induced IL-17a and NO production by cells from the peritoneal cavity, and M1 marker expression predominated on peritoneal macrophages. These cells are also more prone to producing TNF-α, IL-6 and NO when infected by T. cruzi and show high trypanocidal capacity. Due to a hostile peritoneal microenvironment caused by Con-A, which induces macrophage cNOS and iNOS expression, infected BALB/c mice showed reduced parasitemia and an increased survival rate.
Significance: We conclude that Con-A can induce peritoneal M1 macrophage polarization to increase trypanocidal activity, resulting in ameliorated systemic infection in a susceptible experimental model.
(Copyright © 2020 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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