Scholarship 23/07194-7 - Inflamassomos, Leishmania - BV FAPESP
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Function of NALP12 an miR-294 in the macrophage activation and susceptibility to infection with Leishmania amazonensis

Grant number: 23/07194-7
Support Opportunities:Scholarships in Brazil - Master
Start date until: February 01, 2024
End date until: August 31, 2025
Field of knowledge:Biological Sciences - Parasitology
Principal Investigator:Sandra Marcia Muxel
Grantee:Clara Andrade Teixeira
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

In this project, we aim to evaluate the function of NALP12 and microRNA-294 in regulating the response of macrophages infected with L. amazonensis. We hypothesized that infection with L. amazonensis changes the expression of the NLR family, pyrin domain containing 12 (NALP12) and the microRNA encoded in the antisense strand into NALP12 gene, microRNA-294. The set of signals mediated by these molecules alter inflammasome activation and cytokine production in macrophages, increasing susceptibility to infection. NALP12 is a member of the NLR family, involved in the activation of NF-ºB and caspase-1, downregulating inflammasome and inflammatory response in macrophages, T cells, and other immune cells. The miR-294 family is transcribed from the antisense strand of the Nalp12 gene in mice (Mus musculus). The miRNAs are small endogenous noncoding RNAs not translated into proteins, which regulate gene expression by pairing their seed (6-9 nt) with the complementary 3'UTR sequence of the target mRNA, promoting the degradation or inhibition of mRNA translation. In the previous data from our group, we observed increased levels of miR-294 and regulation of Tnf, Mcp-1 and Nos2 mRNA, reducing NO production and increasing infection with L. amazonensis in BALB/c macrophages. Therefore, it is important to understand the correlation between the expression of NALP12 and miR-294 in Leishmania-infected macrophages and how the modulation of these molecules impact in the activation of the pro-inflammatory response and subversion of the host's response to the parasite.

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