Differential ability to resist to complement lysis and invade host cells mediated by MBL in R4 and 860 strains of Trypanosoma cruzi. Issue 6 (19th February 2014)

• Record Type: Journal Article
• Authors: Evans-Osses, Ingrid; Mojoli, Andres; Beltrame, Marcia Holsbach; da Costa, Denise Endo; DaRocha, Wanderson Duarte; Velavan, Thirumalaisamy P.; de Messias-Reason, Iara; Ramirez, Marcel Ivan
• Is Part Of: FEBS letters. Volume 588:Issue 6(2014)
• Page Start: 956
• Page End: 961
• Publication Date: 2014-02-19
• Subjects: Mannan binding lectin -- Complement system -- Chagas disease -- Inate immunity -- Parasite–host cell interaction; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.01.054
• Languages: English
• ISSNs: 0014-5793

Abstract

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. Abstract : MBL has a central role in the activation of Complement Lectin Pathway. Trypanosoma cruzi displays strains resistant or sensitive to complement Lysis. The resistant to complement lysis could be crucial to proceed with the infection. Dual role of MBL in invasion: facilitating entry or as complement activator.