Differential ability to resist to complement lysis and invade host cells mediated by MBL in R4 and 860 strains of Trypanosoma cruzi |
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| Authors: | Ingrid Evans-Osses Andres Mojoli Marcia Holsbach Beltrame Denise Endo da Costa Wanderson Duarte DaRocha Thirumalaisamy P Velavan Iara de Messias-Reason Marcel Ivan Ramirez |
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| Institution: | 1. Laboratório de Biologia Molecular de Parasitas e Vetores, Instituto Oswaldo Cruz – Fiocruz., Av Brasil, 4550. Manguinhos-Rio de Janeiro, Brazil;2. Laboratório de Imunopatologia Molecular, Departamento de Patologia Médica, Universidade Federal do Paraná, Curitiba, Brazil;3. Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany;4. Laboratório de Genômica Funcional de Parasitos, Departamento de Bioquimica e Biologia Molecular, Universidade Federal de Parana, Curitiba, Brazil |
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| 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. |
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| Keywords: | Mannan binding lectin Complement system Chagas disease Inate immunity Parasite&ndash host cell interaction |
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