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Shining a light on molecular mechanisms that potentiate phagocytosis of bacteria

Project description

When immunity shields infection

Antibiotics revolutionised medicine, but bacterial infections remain one of the world’s most persistent killers. While drug-resistant ‘superbugs’ get most of the attention, they are not the only threat. New research shows that bacteria like Staphylococcus aureus can actually retreat inside our own immune cells to survive. By using these cells as shields, pathogens can hide from antibiotics and lie dormant, only to resurface long after treatment ends. The ERC-funded ImmunoSynergy project aims to map the interaction between pathogens and the immune system’s internal structures in real-time using ultra-high-resolution imaging. The goal is to develop new therapies that prevent pathogens from nesting. This approach bridges the gap between immunity and medicine to stop relapsing infections before they start.

Objective

Antibiotics are among the greatest medical achievements of the 20th century and have significantly extended human lifespan. Nevertheless, bacterial infectious diseases continue to be a leading cause of death worldwide. Antibiotic treatment failures are common and typically linked to antimicrobial resistance (AMR), though resistance genes are not always present in such cases. Innate immune cells, particularly phagocytes serve as the first line of defence against infection, but they can paradoxically become reservoirs for certain pathogens. Within host cells, these bacteria are shielded from many antibiotic classes and may adopt persister phenotypes that confer tolerance, enabling them to survive phagocytosis and reinfect patients.

My conviction is that tackling AMR and tolerance requires sophisticated approaches, where we need to find complementary pathways between immune response and antibiotic activity. Recent advances in super-resolution imaging will allow me to scrutinise molecular mechanisms in both host and pathogen that directly influence the outcome of phagocytosis. I propose to i), develop a super-resolution model of phagocytosis, using major AMR pathogen Staphylococcus aureus and host Drosophila melanogaster, to provide ground-breaking insights into the mechanisms of infection; ii), investigate how bacteria coordinate the cell cycle during infection, to identify vulnerabilities and test strategies to kill the internalised pathogens and iii), explore the roles of the host centrosome during phagocytosis, to determine how this organelle regulates the cytoskeleton and assess its potential as a target for immunomodulation.

I will harness cutting-edge imaging technology to significantly advance the field of host-pathogen interactions. My main objective is to identify molecular targets and pathways that potentiate phagocytosis of bacteria and use that knowledge to develop synergistic therapies, which I hope can help reduce the global burden of AMR.

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HORIZON-ERC - HORIZON ERC Grants

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(opens in new window) ERC-2025-STG

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Host institution

THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 2 495 392,08
Address
WELLINGTON SQUARE UNIVERSITY OFFICES
OX1 2JD Oxford
United Kingdom

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Region
South East (England) Berkshire, Buckinghamshire and Oxfordshire Oxfordshire
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 2 495 392,08

Beneficiaries (1)

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