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Role of STING pathway in interplay with TNF signalling and glucose metabolism during malaria

Grant number: 23/10325-6
Support Opportunities:Scholarships abroad - Research Internship - Post-doctor
Effective date (Start): September 18, 2023
Effective date (End): January 31, 2024
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:João Santana da Silva
Grantee:Kely Catarine Matteucci
Supervisor: Nicolas Riteau
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), France  
Associated to the scholarship:20/01043-9 - Immunological mechanisms of resistance and disease in Malaria, BP.PD

Abstract

Malaria, caused by parasites from the genus Plasmodium, remains a major global health concern with millions of reported cases and deaths annually. The innate immune response involves PRRs that recognize malarial PAMPs and DAMPs, including those that promote the activation of cGAS-STING pathway. STING plays a pivotal role in immune responses against Plasmodium, inducing type I interferons and pro-inflammatory responses. Additionally, TNF signaling also interacts with STING and regulates its activity, affecting the immune response against Plasmodium. Both STING and TNF activation in response to parasite influence pathogenesis and immune defense during malaria. In our research project, developed in Brazil (FAPESP process number 2020/01043-9), we showed that TNF is involved in the induction of GLUT-1 expression in monocytic cells, which depends on the inducible nitric oxide synthase (iNOS) expression and stabilization of HIF-1±. The complex interplay between TNF, STING and cellular metabolism during malaria requires further investigation to elucidate their roles in the pathogenesis of the disease, which can reveal future potential therapeutic targets. Our aim here is to investigate the interplay between STING pathway and TNF signaling in the modulation of glucose metabolism in myeloid cells using Hemozoin and malarial DNA to mimic Plasmodium infection. (AU)

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