Proteolytic cleavage of chemokines by Trypanosoma cruzi’s cruzipain inhibits chemokine functions by promoting the generation of antagonists

I. BENITEZ-HERNANDEZ, E. MENDEZ-ENRIQUEZ, P. OSTOA, T. FORTOUL, J.A. RAMIREZ, C. STEMPIN, F. CERBAN, G. SOLDEVILA, E.A. GARCIA-ZEPEDA.

Elsevier

Lugar: Leicester, U.K.; Año: 2010 vol. 215 p. 143 - 143

hagas disease is a chronic inflammatory disease caused by infection with Trypanosoma cruzi. Although it had a decline in recent years, it still affects millions of people in Latin America. The host immune response against this parasite is complex and relies on the development of an efficient T cell-mediated response; however, T. cruzi displays a number of evasion mechanisms allowing it to remain undetected even for years. One of these is the secretion of antiinflammatory molecules such as proteases and the modulation of biological functions of chemokines. Our objective was to analyze the effect of a major cysteine protease, cruzipain, on a number of critical functions of several CC chemokines, both in vitro and in vivo. Initially, using a murine model of T. cruzi infection, we demonstrated that CCL-2 and CCL-12 chemokines are highly expressed at different stages and correlated with an increase in the expression of cruzipain. In addition, we demonstrated that cruzipain is capable of di