Differential ability to resist to complement lysis and invade host cells mediated by MBL in R4 and 860 strains of Trypanosoma cruzi

Abstract

a b s t r a c tTo 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 complementmediated 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.

Recently differentiated epimastigotes from Trypanosoma cruzi are infective to the mammalian host

“…Flow cytometry analysis of parasite lysis (Fig. A and B) indicated epimastigote lysis kinetics very similar to those already shown for other T. cruzi strains (Cestari et al ., ; Evans‐Osses et al ., ), with 91 and 100% lysed cells after 15 and 30 min of FHS exposure (Fig. B).…”

“…As we used nonimmune serum, and the Ca ++ chelating agent EGTA strongly inhibits epimastigote killing (Fig. B), parasite lysis was most likely mediated primarily by the lectin pathway of complement activation, as already shown (Cestari and Ramirez, , ; Evans‐Osses et al ., ).…”

“…Trypanosoma cruzi rdEpi are infective to mammal 727 activated route for T. cruzi killing in non-immune serum (Cestari et al, 2009;Cestari and Ramirez, 2010;Evans-Osses et al, 2014). Classically, T. cruzi epimastigotes were the only parasite form that exhibited total susceptibility to complement killing (Cestari et al, 2009;Evans-Osses et al, 2014). Epimastigotes were also considered the only parasite form that is totally destroyed inside the macrophage phagolysosome (de Carvalho and de Souza, 1989;Cohn, 1976, 1977).…”

Mannose-binding Lectin (MBL) as a susceptible host factor influencing Indian Visceral Leishmaniasis

“…In addition, three non-synonymous [18]. Lectin complement proteins have been associated with many infectious diseases including intra and extracellular infections [22][23][24][25]. Our earlier study has shown that, another analogous lectin complement protein ficolin-2 was associated with occurrence of VL [26].…”

Collectins: Innate Immune Pattern Recognition Molecules

“…In a mouse model of T. cruzi infection, MBL influences host resistance and pathology (Rothfuchs et al 2012). In some strains of T. cruzi, MBL mediates resistance to complement lysis of the parasite and enhances invasion of host cells (Evans-Osses et al 2014).…”