Differential ability to resist to complement lysis and invade host cells mediated by MBL in R4 and 860 strains of Trypanosoma cruzi.
FEBS Lett
; 588(6): 956-61, 2014 Mar 18.
Article
in En
| MEDLINE
| ID: mdl-24560788
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.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Trypanosoma cruzi
/
Protozoan Proteins
/
Mannose-Binding Lectin
Limits:
Animals
/
Humans
Language:
En
Journal:
FEBS Lett
Year:
2014
Document type:
Article
Affiliation country:
Brazil