Claude Libert Lab

Research focus

The main goal of our research is to contribute to the understanding of the molecular mechanisms that are involved in the progression of sepsis. Sepsis is a deadly disease that is initiated by a (bacterial) infection and leads to a severe host response. It hits 30 million people yearly, 8 million of which die (3 million children). The savage, acute and complex nature of sepsis has caused much confusion as to the most relevant molecular mechanisms involved. Since many clinical trials for sepsis have failed, the classical belief that sepsis is primarily inflammatory in nature is under pressure. In our group, we focus our attention on metabolic reprogramming in sepsis, which we think follows a pattern that is compatible with an extremely acute starvation response, but which fails due to the inhibition of the function of several important transcription factors, such as the Glucocorticoid Receptor and PPAR. The molecular pathways that undermine these factors form a central theme in our research.

Next to this metabolic project, we are also interested in the control of host-pathogen interplay between microbes of the gut and the Paneth cells in the ileum. This interaction is important in defining the composition of these microbes, as well as the sensitivity of intestinal cells for inflammation and cell death. We are focusing on the interaction between bacteria and Paneth cells, and the role of interferons in this interplay and the impact of zinc and other nutrients on this axis. 

Finally, because we are applying mice as model animals, we are interested in the details of the mouse genome and which naturally occurring alleles of protein-coding genes and micro
RNA genes are available in the 40 dee- sequenced mouse strains and the role that these variant alleles play in phenotypes of interest in the mouse strains. 

Area of expertise

  • Cytokine biology
  • Sepsis models in mice
  • Metabolism
  • Liver biology
  • Nuclear receptors
  • Generation of mouse mutants
  • Mapping and cloning traits in mice
  • Genomics and transcriptomics

Publications

TNF-a inhibits glucocorticoid receptor-induced gene expression by reshaping the GR nuclear cofactor profile.Dendoncker K, Timmermans S, Vandewalle J, Eggermont M, LEMPIAINEN , PAAKINAHO , Van Hamme E, Dewaele S, Vandevyver S, Ballegeer M, Souffriau J, Van Wyngene L, Van Looveren K, Vanderhaeghen T, Beyaert R, De Bosscher K, PALVIMO , Van Montagu M, Libert CPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 116, 12942-12951, 2019
Glucocorticoid receptor dimers control intestinal STAT1 and TNF-induced inflammation in miceBallegeer M, Van Looveren K, Timmermans S, Eggermont M, VANDEVYVER , Thery F, Dendoncker K, Souffriau J, Vandewalle J, Van Wyngene L, De Rycke R, Takahashi N, Vandenabeele P, TUCKERMANN , REICHARDT , Impens F, Beyaert R, De Bosscher K, Vandenbroucke R, Libert CJOURNAL OF CLINICAL INVESTIGATION, 128, 3265-3279, 2018
Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strainsTimmermans S, Van Montagu M, Libert CPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 114, 9158-9163, 2017
Glucocorticoid-induced microRNA-511 protects against TNF by down-regulating TNFR1Puimège L, Van Hauwermeiren F, Steeland S, Van Ryckeghem S, Vandewalle J, Lodens S, Dejager L, Vandevyver S, Staelens J, Timmermans S, Vandenbroucke R, Libert CEMBO MOLECULAR MEDICINE, 7, 1004-17, 2015
Safe TNF-based antitumor therapy following p55TNFR reduction in intestinal epitheliumVan Hauwermeiren F, ARMAKA , KARAGIANNI , KRANIDIOTI , Vandenbroucke R, Loges S, Van Roy M, Staelens J, Puimège L, PALAGANI , VANDEN , VICTORATOS , Carmeliet P, Libert C, KOLLIAS JOURNAL OF CLINICAL INVESTIGATION, 123, 2590-603, 2013

Job openings

News

Check your favorite mouse genes in mousepost.be

08/08/2017 - ​VIB scientists at Ghent University uncover and display (mousepost.be = mouse polymorphic sequence tags) the full richness of the mouse protein-coding genome for the mouse community.

New Horizon 2020 Project B-SMART Develops RNA-based Therapy for Neurodegenerative Diseases

01/02/2017 - Neurodegenerative diseases such as Alzheimer’s affect over 7 million people in Europe – a figure which is expected to double every 20 years as the population ages and thus poses a significant healthcare burden to European society.

Belgian scientists discover missing link in septic shock

14/09/2016 - VIB & Ghent University Researchers discovered important mechanism of sepsis, an overreaction of the body’s immune system to an infection. In this condition, the brain is unable to curb an inflammatory response, causing organ failure or ‘septic shock’.

Disruption of brain-blood barrier might influence progression of Alzheimer’s

29/09/2015 - The team of Roosmarijn Vandenbroucke in the Claude Libert Group (VIB/UGent) combined their knowledge and expertise related to inflammation with the expertise in Alzheimer’s disease present in the Bart De Strooper Group (VIB/KU Leuven).

Various avenues to counteract TNF - crucial to tackling acute inflammation

25/08/2015 - ​The cytokine TNF plays and important role in acute inflammation and in a number of auto-immune conditions. TNF needs to pass on a signal in order to execute its role. This can be achieved by binding to a receptor.

New breakthroughs in TNF biology

19/09/2013 - Two new stories from the group of Claude Libert (VIB - UGent) increase our knowledge about the mechanism of TNF release, the role of the gutin TNF’s acute toxicity and the value of TNFR1 as adrug target.

Claude Libert

Claude Libert

Research area(s)

Model organism(s)

Bio

​PhD: Ghent University, Ghent, Belgium, 1993
Postdoc: Instituto di Ricerche di Biologia Molecolare, Rome, Italy
VIB Group leader since 1997

Contact Info

VIB-UGent Center for Inflammation ResearchUGent-VIB Research Building FSVMTechnologiepark 71 9052 GENTRoute description