Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/10193
Title: Differential ability to resist to complement lysis and invade host cells mediated by MBL in R4 and 860 strains of Trypanosoma cruzi
Authors: Evan-Osses, Ingrid
Mojoli, Andres
Beltrame, Marcia Holsbach
Costa, Denise Endo da
Rocha, Wanderson Duarte da
Velavan, Thirumalaisamy O
Reason, Iara de Messias
Ramirez, Marcel Ivan
Affilliation: Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Molecular de Parasitas e Vetores. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Molecular de Parasitas e Vetores. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Paraná. Departamento de Patologia Médica. Laboratório de Imunopatologia Molecular. Curitiba, PR, Brasil.
Universidade Federal do Paraná. Departamento de Patologia Médica. Laboratório de Imunopatologia Molecular. Curitiba, PR, Brasil.
Universidade Federal do Paraná. Departamento de Bioquímica e Biologia Molecular. Laboratório de Genômica Funcional de Parasitos. Curitiba, PR, Brasil.
University of Tübingen. Instituto of Tropical Medicine. Tübingen, Germany.
Universidade Federal do Paraná. Departamento de Patologia Médica. Laboratório de Imunopatologia Molecular. Curitiba, PR, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Molecular de Parasitas e Vetores. Rio de Janeiro, RJ, Brasil.
Abstract: To produce an infection Trypanosoma cruzi must evade lysis by the complement system. During early stages of infection, the lectin pathway plays an important role in host defense and can be activated by binding of mannan-binding lectin (MBL) to carbohydrates on the surface of pathogens. We hypothesized that MBL has a dual role during parasite-host cell interaction as lectin complement pathway activator and as binding molecule to invade the host cell. We used two polarized strains of T. cruzi, R4 (susceptible) and 860 (resistant) strains, to investigate the role of MBL in complement-mediated lysis. Interestingly R4, but not 860 metacyclic strain, markedly increases the invasion of host cells, suggesting that MBL drives the invasion process while the parasite deactivates the Lectin complement pathway.
Keywords: Mannan binding lectin
Complement system
Chagas disease
Inate immunity
Parasite–host cell interaction
Keywords in spanish: Enfermedad de Chagas
keywords: Doença de Chagas
Issue Date: 2014
Publisher: Elsevier
Citation: EVAN-OSSES, Ingrid et al. Differential ability to resist to complement lysis and invade host cells mediated by MBL in R4 and 860 strains of Trypanosoma cruzi. FEBS Letters v.588, n.6, p.956–961, 2014.
DOI: 10.1016/j.febslet.2014.01.054
ISSN: 0014-5793
Copyright: open access
Appears in Collections:IOC - Artigos de Periódicos

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