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Inflammafish

Cross-talk between inflammation and autophagy in tuberculosis

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EC-Contrib. €

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Partnership

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Project "Inflammafish" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITEIT LEIDEN 

Organization address
address: RAPENBURG 70
city: LEIDEN
postcode: 2311 EZ
website: www.universiteitleiden.nl

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 Netherlands [NL]
 Project website https://www.universiteitleiden.nl/en/research/research-projects/science/ibl-inflammafish-cross-talk-between-inflammation-and-autophagy-in-tuberculosis
 Total cost 177˙598 €
 EC max contribution 177˙598 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-01-18   to  2018-01-17

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITEIT LEIDEN NL (LEIDEN) coordinator 177˙598.00

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 Project objective

The increasing occurrence of multidrug-resistant Mycobacterium tuberculosis strains makes tuberculosis (TB) a key priority for infectious disease research. Inflammation and autophagy are two fundamental processes critical to TB pathogenesis. Accumulating evidence shows that TB disease is worsened by deregulation of the inflammatory response. On the other hand, autophagy has recently emerged as a crucial host defence mechanism. Autophagy counteracts the ability of mycobacteria to survive inside host cells and targets them for degradation. Autophagy is also thought to control the inflammatory response. However, the interaction between inflammation and autophagy in host defence against TB remains unclear. The aim of my proposal is to use the well-established zebrafish model of TB to gain insight into this key question. Recently, the host laboratory discovered that the DNA damage-regulated autophagy modulator (DRAM1) protects against TB in the zebrafish model. They also implicated this important autophagy regulator in inflammation, as it strongly affects expression of interleukin-1beta (IL1B). I have specific expertise in studying IL1B-mediated inflammation in zebrafish. Thus the proposed project will be a great synergy between me and the host laboratory, which is leading in zebrafish infectious disease research. I will determine how modulation of autophagy or manipulation of IL1B levels reciprocally influence each other during TB disease. The zebrafish model provides excellent tools to visualize these processes in vivo. Furthermore, I will take advantage of the host’s expertise in RNA sequencing and proteomics to study genome-wide effects of autophagy modulation on the inflammatory response. A secondment will allow me to compare results in the TB model with a damage-induced inflammation model. The project will provide new insights into regulatory pathways that could potentially be intervened in treatment of TB or other inflammatory diseases with common characteristics.

 Publications

year authors and title journal last update
List of publications.
2018 Nadja R. Brun, Bjørn E. V. Koch, Mónica Varela, Willie J. G. M. Peijnenburg, Herman P. Spaink, Martina G. Vijver
Nanoparticles induce dermal and intestinal innate immune system responses in zebrafish embryos
published pages: , ISSN: 2051-8153, DOI: 10.1039/C8EN00002F
Environmental Science: Nano 2019-06-17

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

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