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Investigating if recuperating hepatic macrophage numbers and functions in chronic fibrosis can limit the incidence and severity of infections

Project description

Understanding increased susceptibility to infections in fibrosis patients

Liver fibrosis, the build-up of scar tissue that impairs liver function, is often caused by viral hepatitis, alcohol abuse, or obesity. It is dangerous for patients as it makes them more susceptible to infections. Unfortunately, the reasons behind this increased susceptibility are not well understood, which hinders the development of solutions or treatments. Supported by the Marie Skłodowska-Curie Actions programme, the ReKUPFFERate project will study a subset of macrophages that are immune cells responsible for eliminating pathogens in the liver. The project will focus on Kupffer cells, a type of macrophage that is found in fewer numbers in fibrotic livers. The research will explore the hypothesis that this altered macrophage landscape contributes to the increased infection susceptibility in fibrosis.

Objective

Liver fibrosis is the build-up of scar tissue resulting in impaired liver function. It can have different causes including alcohol abuse, obesity and viral hepatitis. For reasons that we do not fully understand, patients with fibrosis (termed cirrhosis) are more susceptible to infections. In fact, 50% of hospitalized patients with liver cirrhosis and infection die, highlighting the scale of this problem. Macrophages (MFs) are immune cells present in every tissue of the body that function to eliminate pathogens. In the liver, one subset of MFs, the Kupffer cells (KCs) are perfectly equipped with scavenger and pathogen recognition receptors to do this. Moreover, they are positioned in the bloodstream meaning they are one of the first cells to sense and respond to circulating pathogens although their precise roles have not yet been elucidated. In cirrhosis, KCs are reduced in number, being replaced by distinct MF subtypes, including a population termed lipid-associated MFs (LAMs). Preliminary data from the host lab demonstrate that both KCs and LAMs from the cirrhotic liver respond less efficiently to infection when compared with their healthy counterparts. Thus, I hypothesize that the altered MF landscape in cirrhosis and fibrosis is one mechanism driving the increased susceptibility and exacerbated responses to infection in these patients. Here, I aim to test this hypothesis by examining how the different MFs respond to infection in the presence and absence of fibrosis. Using novel mouse models specifically targeting the distinct MF populations, coupled with ex vivo cultures of human hepatic MFs, I will tease apart the mechanisms through which MFs exert their effects and attempt to manipulate these to recuperate normal MF numbers and functions potentially uncovering novel therapeutic approaches to limit infection and improve cirrhotic patient health.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2022-PF-01

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Coordinator

VIB VZW
Net EU contribution

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€ 175 920,00
Address
SUZANNE TASSIERSTRAAT 1
9052 ZWIJNAARDE - GENT
Belgium

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Region
Vlaams Gewest Prov. Oost-Vlaanderen Arr. Gent
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Research Organisations
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