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ENTRI SIGNED

Enteric-nervous-system-mediated regulation of intestinal inflammation

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 ENTRI project word cloud

Explore the words cloud of the ENTRI project. It provides you a very rough idea of what is the project "ENTRI" about.

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Project "ENTRI" data sheet

The following table provides information about the project.

Coordinator
CHARITE - UNIVERSITAETSMEDIZIN BERLIN 

Organization address
address: Chariteplatz 1
city: BERLIN
postcode: 10117
website: www.charite.de

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Total cost 1˙499˙638 €
 EC max contribution 1˙499˙638 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-STG
 Funding Scheme ERC-STG
 Starting year 2019
 Duration (year-month-day) from 2019-07-01   to  2024-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    CHARITE - UNIVERSITAETSMEDIZIN BERLIN DE (BERLIN) coordinator 1˙499˙638.00

Map

 Project objective

Environmental and internal stimuli are constantly sensed by the body’s two large sensory units, the nervous system and the immune system. Integration of these sensory signals and translation into effector responses are essential for maintaining body homeostasis. While some of the intrinsic pathways of the immune or nervous system have been investigated, how the two sensory interfaces coordinate their responses remains elusive. We have recently investigated neuro-immune interaction at the mucosa of the intestine, which is densely innervated by the enteric nervous system (ENS). Our research has exposed a previously unrecognized pathway used by enteric neurons to shape type 2 immunity at mucosal barriers. Cholinergic enteric neurons produce the neuropeptide Neuromedin U (NMU) to elicit potent activation of type 2 innate lymphoid cells (ILC2s) via Neuromedin U receptor 1, selectively expressed by ILC2s. Interestingly, NMU stimulated protective immunity against the parasite Nippostrongylus brasiliensis but also triggered allergic lung inflammation. Therefore, the NMU-NMUR1 axis provides an excellent opportunity to study how neurons and immune cells interact to regulate immune responses and maintain body homeostasis. We propose to generate and use elegant genetic tools, which will allow us to systematically investigate the consequences of neuro-immune crosstalk at mucosal surfaces in various disease models. These tools will enable us to selectively measure and interfere with neuronal and ILC2 gene expression and function, thereby leading to an unprecedented understanding of how the components of neuro-immune crosstalk contribute to parasite immunity or allergic disease development. Furthermore, we will progress into translational aspects of NMU-regulated immune activation for human immunology. Therefore, our research has the potential to develop basic concepts of mucosal immune regulation and such discoveries could also be harnessed for therapeutic intervention.

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The information about "ENTRI" are provided by the European Opendata Portal: CORDIS opendata.

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