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iMAC-FUN

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Dissecting novel mechanisms of iron regulation during macrophage fungal interpla...

Dissecting novel mechanisms of iron regulation during macrophage fungal interplay Airborne filamentous fungi (molds) are major causes of respiratory diseases in an expanding population of patients with complex immune and metabolic defects. Invasive mold infections (IMI) are associated with substantial mortality... ver más

31/08/2025

FOUNDATION FOR RES...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

IDRYMA TECHNOLOGIAS KAI EREVNAS No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

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Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2020-06-09

ERC-2019-COG: ERC Consolidator Grant

I+D

Cerrada hace 5 años

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2 Participantes

FOUNDATION FOR RESEARCH AND...

2.00M€ | Lider

SELENA IBERIA

169.74K€ | Participante

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Duración del proyecto: 62 meses Fecha Inicio: 2020-06-09
Fecha Fin: 2025-08-31

Líder del proyecto

IDRYMA TECHNOLOGIAS KAI EREVNAS No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Airborne filamentous fungi (molds) are major causes of respiratory diseases in an expanding population of patients with complex immune and metabolic defects. Invasive mold infections (IMI) are associated with substantial mortality and enormous economic impact. Understanding pathogenesis of IMI is an unmet need for design of better therapies. We have put forward a novel mechanism for the pathogenesis of IMI, according to which development of IMI requires two discrete mechanisms (a) phagosome maturation arrest via inhibition of LC3-associated phagocytosis (LAP), which allows intracellular persistence of fungal conidia (spores), and (b) alteration in iron homeostasis, resulting in invasive fungal growth and lysis of the macrophage. On the pathogen site, fungal melanin targets LAP and affects macrophage metal homeostasis. On the macrophage site, iron distribution in subcellular compartments of all eukaryotic cells is controlled by ferric reductases and divalent cation transporters, in a process that remains molecularly unexplored. During mold infection a group of ferric reductases represent the most prominently transcriptionally modulated iron regulatory genes in macrophages. Thus, iron regulation is the critical determinant of macrophage-fungal interplay and is the focus of this project. We will use molds as model pathogens to (i) dissect the role of selected ferric reductases in infection, (ii) identify novel iron transporters implicated in host defense (iii) and explore mechanisms of melanin interference with iron regulation in macrophages. To this end, we will employ a robust, unbiased, approach combining transcriptomics, metalloproteomics, in vivo RNAi screening in Drosophila model of IMI, and validation studies in transgenic mice and eventually in human patients ex vivo. Dissecting the function of novel iron regulators in the macrophage will have profound impact on iron biology and is likely to have direct therapeutic implications for the management of IMI.

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