1. NLRP3 Inflammasome and Caspase-1/11 Pathway Orchestrate Different Outcomes in the Host Protection Against Trypanosoma cruzi Acute Infection.

PAROLI A; GONZALES PV; DIAZ LUJAN C; ONOFRIO L; AROCENA A; AROCENA A; CARRERA SILVA EA; GEA S

Frontiers in Immunology

Frontiers Research Foundation

Año: 2018

1664-3224

nfection with protozoan parasite Trypanosoma cruzi results in activation of nucleotide binding domain and leucine-rich repeat containing receptors (NLRs). NLR activation leads to inflammasome formation, the activation of caspase-1, and the subsequent cleavage of IL-1β and IL-18. Considering that inflammasome activation and IL-1β induction by macrophages are key players for an appropriate T cell response, we investigated the relevance of NLR pyrin domain-containing 3 (NLRP3) and caspase-1/11 to elucidate their roles in the induction of different T cell phenotypes and the relationship with parasite load and hepatic nflammation during T. cruzi-Tulahuen strain acute infection. Wedemonstrated that infected nlrp3−/− and C57BL/6 wild type (WT) mice exhibited similar parasitemia and survival, although the parasite load was higher in the livers of nlrp3−/− mice than in those of WT mice. Increased levels of transaminases and pro-inflammatorycytokines were foun