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TANK_Sepsis

Financiado

Targeting Amino acid uptake into NK cells to limit pathogenesis in sepsis

Sepsis is a global health challenge, accounting for around 20% of deaths worldwide. While sepsis is induced by uncontrolled dissemination of infection, significant contribution to disease pathogenesis is made by overwhelming produ... ver más

30/09/2025

TRINITY COLLEGE DU...

216K€

Presupuesto del proyecto: 216K€

Líder del proyecto

THE PROVOST FELLOWS FOUNDATION SCHOLARS THE... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2023-04-18

HORIZON-MSCA-2022-PF-01-01: MSCA Postdoctoral Fellowships 2022 ExpectedOutcome:

I+D

Cerrada hace 2 años

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1 Participantes

TRINITY COLLEGE DUBLIN

215.53K€ | Lider

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Duración del proyecto: 29 meses Fecha Inicio: 2023-04-18
Fecha Fin: 2025-09-30

Líder del proyecto

THE PROVOST FELLOWS FOUNDATION SCHOLARS THE... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 216K€

Descripción del proyecto Sepsis is a global health challenge, accounting for around 20% of deaths worldwide. While sepsis is induced by uncontrolled dissemination of infection, significant contribution to disease pathogenesis is made by overwhelming production of proinflammatory mediators, a so-called cytokine storm. There is a pressing need for new target therapies to dampen this immunopathogenesis while still allowing bacterial clearance. Although Natural Killer (NK) cells are vital for host innate responses, they are important contributors to the tissue damage during bacterial sepsis, in particular, via production of excessive amounts of IFNg. Therefore, dampening NK cell IFNg production represents a promising tool for sepsis treatment. Recent studies from the host institution have shown that metabolic processes are essential for NK cell functions. In particular, certain amino acid transporters are key to support IFNg expression by NK cells. I thus hypothesize that limiting amino acid supply to NK cells will restrict production of IFNg, dampen the cytokine storm, and improve the course of bacterial sepsis. To prove this idea, I will combine my experience in mouse models of septic shock with host institution’s background on immunometabolism and bacterial infections. First, I will employ a powerful metabolic toolbox established at the supervisor’s lab to characterize metabolic phenotype of NK cells in bacterial sepsis. Next, I will use mice with genetic ablation of key amino acid transporters specifically in NK cells to study their role in cytokine storm during sepsis. Finally, I will test pharmacological compounds, able to limit amino acid availability, for their potential to prevent excessive inflammation during sepsis. At the end of the project, I will acquire key professional skills, including metabolic toolbox and bacterial infection model, that will benefit my further career, as well as characterize new potential therapeutic opportunity for treatment of sepsis.

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