H2020Индивидуална стипендия2016–2018

Inflammafish · Cross-talk between inflammation and autophagy in tuberculosis

„Хоризонт 2020“ — Действия „Мария Склодовска-Кюри“

Период: 2016-01-18 → 2018-01-17
Финансиране от ЕС: 177 599 €
Участници: 1
Схема: MSCA-IF-EF-ST

Линиите свързват координатора с партньорите.

Накратко на български

Взаимодействието между възпалението и процеса на самоизчистване (автофагия) при туберкулоза се изучава чрез ембриони на зебра риба. Това помага да се разбере как тялото се защитава от бактерии, които стават устойчиви на лекарства.

Този кратък обзор е генериран от изкуствен интелект

Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.

Резултати накратко

Cross-talk between inflammation and autophagy in tuberculosis

The overall aim of the project “Cross-talk between inflammation and autophagy in tuberculosis” was to use the zebrafish embryo as in vivo model to gain understanding of the intercommunication between inflammation and autophagic host defence during Tuberculosis (TB). The increasing occurrence of multidrug-resistant Mycobacterium tuberculosis strains makes 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 deregulations of the inflammatory response. On the other hand, autophagy has recently emerged as a crucial host defence mechanism. Autophagy is also thought to control the inflammatory response. However, the interaction between inflammation and autophagy in host defence against TB remains unclear. The specific objectives of this project included studying the effect of autophagy modulation on the inflammatory response, determining the effect that the modulation of the inflammatory response has on autophagy, but also studying genome-wide effects of autophagy modulation using RNA sequencing and proteomics during the infection and under basal condition.

Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз

Цел на проекта

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.

Оригинален текст от CORDIS (на английски).

Участници

UNIVERSITEIT LEIDEN · LeidenКоординаторНидерландия