| Grant number: | 16/01917-3 |
| Support Opportunities: | Regular Research Grants |
| Start date: | September 01, 2016 |
| End date: | August 31, 2018 |
| Field of knowledge: | Health Sciences - Medicine |
| Principal Investigator: | Ana Claudia Trocoli Torrecilhas |
| Grantee: | Ana Claudia Trocoli Torrecilhas |
| Host Institution: | Instituto de Ciências Ambientais, Químicas e Farmacêuticas (ICAQF). Universidade Federal de São Paulo (UNIFESP). Campus Diadema. Diadema , SP, Brazil |
| City of the host institution: | Diadema |
Abstract
Infective forms of Trypanosoma cruzi, the causative agent of Chagas disease release vesicles enriched with glycoproteins that when injected into mice modulate parasite infection. The vesicles released by trypomastigotes of Y strain increases parasitism and inflammation of the heart tissue via the action of TNF-±, IL-12 and NO. Nogueira et al (2015) showed that vesicles isolated from YuYu, CL-14 and Y strains induced NO production, TNF-± and IL-6 via TLR2. Vesicles from Colombiana strain induced levels below the threshold of detection of these pro-inflammatory cytokines and NO. Vesicles of all analyzed strains activated the MAPK signaling pathway, but this activation was delayed in Colombian strain, explaining the low production of pro-inflammatory cytokines. Those results showed that vesicles released by trypomastigotes of different isolates caused cellular pro-inflammatory stimulation at various levels via the TLR2 receptor, which can be related to the progress of infection in each of the various strains. The objective of this study is to understand how vesicles released by macrophage infected with T. cruzi activate the immune response and inflammation. (AU)
| Articles published in Agência FAPESP Newsletter about the research grant: |
| More itemsLess items |
| TITULO |
| Articles published in other media outlets ( ): |
| More itemsLess items |
| VEICULO: TITULO (DATA) |
| VEICULO: TITULO (DATA) |