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GLYCANS AS MASTER TRIGGERS OF HEALTH TO INTESTINAL INFLAMMATION TRANSITION

Project description

Intestinal carbohydrates: a cause for inflammatory bowel disease?

Inflammatory bowel diseases such as Crohn’s disease (CD) are associated with chronic inflammation of the gut. Emerging evidence indicates that, in patients with CD, intestinal epithelial cells present with aberrant glycosylation and hence perturbed barrier function. The EU-funded GlycanTrigger project is interested in understanding how such changes in gut mucosa glycosylation lead to immune system activation. The working hypothesis is that the perturbations in the glycocalyx – the dense outer layer of carbohydrates of membrane glycolipids and glycoproteins – affect host-microbiome interactions and lead to altered antigens that activate the immune system. Researchers will investigate the presence of anti-glycan antibodies before CD onset as an early indication, aiming to understand the transition to chronic inflammation.

Objective

Chronic inflammation underlies several diseases. In Crohn´s disease (CD), there is mounting evidence of a preclinical phase characterized by immunological changes that precede symptoms. Here, we propose a thorough and innovative approach to better understand the health-to-chronic inflammation transition occurring in patients with CD that will be translated in improved disease prediction and prevention. We will address how changes in glycosylation of the gut mucosa act as a primary event that dysregulates not only local mechanisms (imposing maladapted host-microbiome interactions) but also systemic mechanisms (promoting anti-microbial antibodies production), involving the novel concept of glycan mimicry as an early trigger of the health to inflammation transition – GlycanTrigger. Capitalizing on our recent findings showing that changes in the expression of complex branched N-glycans at gut mucosa regulate Inflammatory Bowel Disease immunopathogenesis, we here hypothesize that changes in gut glycocalyx impose early perturbations in host-microbiome interactions, leading to the exposure of altered (glyco)neoantigens, both by pathogens and host epithelial cells which trigger the activation of innate immune response. Moreover, following our recent discovery that changes in glycosylation can be detected in serum years before CD diagnosis and are correlated with increased levels of pathogenic antimicrobial antibodies (ASCA), we will here pursue the hypothesis that changes in mucosa glycans constitute a major source for the development of anti-glycan antibodies (ASCA), associated with health-to-inflammation transition. The long-term GOAL of this proposal is to unlock, through an integrative approach, a new checkpoint that regulates the transition to chronic inflammation. Our proposal will lead to breakthrough concepts in the health to chronic inflammation transition and to novel predictive tools translated in novel glyco-intervention strategies for disease prevention.

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HORIZON-RIA - HORIZON Research and Innovation Actions

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Call for proposal

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(opens in new window) HORIZON-HLTH-2022-STAYHLTH-02

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Coordinator

I3S - INSTITUTO DE INVESTIGACAO E INOVACAO EM SAUDE DA UNIVERSIDADE DO PORTO
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.

€ 3 478 500,00
Address
RUA ALFREDO ALLEN 208
4200-135 PORTO
Portugal

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Region
Continente Norte Área Metropolitana do Porto
Activity type
Research Organisations
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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.

€ 3 478 500,00

Participants (8)

Partners (1)

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