Trypanosoma cruzi, the causative agent of Chagas disease, modulates interleukine-6-induced

PONCE NE; CARRERA-SILVA AE; PELLEGRINI AV; CAZORLA SI; MALCHIODI EL; LIMA AP; GEA S; AOKI MP

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 2013 vol. 1832 p. 485 - 485

p class="MsoNormal" style="text-align: justify; line-height: 200%; text-indent: 1cm; margin: 0cm -1.75pt 0pt 14.2pt;">Interleukine-6 mediates host defense and cell survival mainly through the activation of the transcription factor STAT3 via the glycoprotein gp130, a shared signal-transducing receptor for several IL-6-type cytokines. We have reported that the cardiotrophic parasite Trypanosoma cruzi protects murine cardiomyocytes from apoptosis. In agreement, an intense induction of the anti-apoptotic factor Bcl-2 is found in cardiac fibers during the acute phase of infection, establishing a higher threshold against apoptosis. We report here that inactive cruzipain, the main cysteine protease secreted by the parasite, specifically triggered TLR2 and