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| Author(s): |
Aramys Silva dos Reis
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2017-03-02 |
| Examining board members: |
Claudio Romero Farias Marinho;
Estela Maris Andrade Forell Bevilacqua;
Karina Ramalho Bortoluci;
Maria Terezinha Serrão Peraçoli;
Alessandra Pontillo
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| Advisor: | Claudio Romero Farias Marinho |
| Abstract | |
Acute respiratory distress syndrome (ARDS) and placental malaria (PM) are complications of the malaria, whose the immunopathogenic mechanisms are poorly understood. In that study we showed that MyD88-/- and Casp 1/11-/- mice did not develop ARDS, dying due to severe anemia associated to hyperparasitemia. Subsequently, it was been shown that although such mechanism depends on the AIM2 inflammasome, it does not depend on the NLRP3 and NLRC4 inflammasomes and the IL-1 axis. In a second stage of the project, it should be noted that those complications are due to the activation of the TLR4/9/MyD88 signaling pathways, but not the TLR2. In addition, the participation of the NLRP3 and AIM2 inflammosomes, but not the NLRC4 was shown in that process. Finally, the data suggest that the activation of these pathways culminates with the release of the IL-1β which acts on its receptor inhibiting the amino acid expression and glucose transporters with a consequent dysfunction in the fetal development of pregnant mice with MP. In conclusion, this work makes for the first time an association between the MyD88 pathway activation and inflammasomes by plasmodium and the progression of the ARDS and MP. (AU) | |
| FAPESP's process: | 11/19048-8 - Role of Inflamassoma in the immunopathogenesis of Placental Malaria |
| Grantee: | Aramys Silva dos Reis |
| Support Opportunities: | Scholarships in Brazil - Doctorate |