Laurent L'Homme
University of Liège
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Publication
Featured researches published by Laurent L'Homme.
Journal of Lipid Research | 2013
Laurent L'Homme; Nathalie Esser; Laura Riva; André Scheen; Nicolas Paquot; Jacques Piette; Sylvie Legrand-Poels
The NLRP3 inflammasome is involved in many obesity-associated diseases, such as type 2 diabetes, atherosclerosis, and gouty arthritis, through its ability to induce interleukin (IL)-1β release. The molecular link between obesity and inflammasome activation is still unclear, but free fatty acids have been proposed as one triggering event. Here we reported opposite effects of saturated fatty acids (SFAs) compared with unsaturated fatty acids (UFAs) on NLRP3 inflammasome in human monocytes/macrophages. Palmitate and stearate, both SFAs, triggered IL-1β secretion in a caspase-1/ASC/NLRP3-dependent pathway. Unlike SFAs, the UFAs oleate and linoleate did not lead to IL-1β secretion. In addition, they totally prevented the IL-1β release induced by SFAs and, with less efficiency, by a broad range of NLRP3 inducers, including nigericin, alum, and monosodium urate. UFAs did not affect the transcriptional effect of SFAs, suggesting a specific effect on the NLRP3 activation. These results provide a new anti-inflammatory mechanism of UFAs by preventing the activation of the NLRP3 inflammasome and, therefore, IL-1β processing. By this way, UFAs might play a protective role in NLRP3-associated diseases.
Biochemical Pharmacology | 2014
Sylvie Legrand-Poels; Nathalie Esser; Laurent L'Homme; André Scheen; Nicolas Paquot; Jacques Piette
Free fatty acids (FFAs) are metabolic intermediates that may be obtained through the diet or synthesized endogenously. In addition to serving as an important source of energy, they produce a variety of both beneficial and detrimental effects. They play essential roles as structural components of all cell membranes and as signaling molecules regulating metabolic pathways through binding to nuclear or membrane receptors. However, under conditions of FFAs overload, they become toxic, inducing ROS production, ER stress, apoptosis and inflammation. SFAs (saturated fatty acids), unlike UFAs (unsaturated fatty acids), have recently been proposed as triggers of the NLRP3 inflammasome, a molecular platform mediating the processing of IL-1β in response to infection and stress conditions. Interestingly, UFAs, especially ω-3 FAs, inhibit NLRP3 inflammasome activation in various settings. We focus on emerging models of NLRP3 inflammasome activation with a special emphasis on the molecular mechanisms by which FFAs modulate the activation of this complex. Taking into consideration the current literature and FFA properties, we discuss the putative involvement of mitochondria and the role of cardiolipin, a mitochondrial phospholipid, proposed to be sensed by NLRP3 after release, exposure and/or oxidation. Finally, we review how this SFA-mediated NLRP3 inflammasome activation contributes to the development of both insulin resistance and deficiency associated with obesity/type 2 diabetes. In this context, we highlight the potential clinical use of ω-3 FAs as anti-inflammatory compounds.
Journal of Innate Immunity | 2017
Hermann Giresse Tima; Juma'a R. Al Dulayymi; Olivier Denis; Pauline Lehebel; Klarah Sherzad Baols; Mohsin O. Mohammed; Laurent L'Homme; Mohaned M. Sahb; Georges Potemberg; Sylvie Legrand; Roland Lang; Rudi Beyaert; Jacques Piette; Mark S. Baird; Kris Huygen; Marta Romano
The cell wall of mycobacteria is characterised by glycolipids composed of different classes of mycolic acids (MAs; alpha-, keto-, and methoxy-) and sugars (trehalose, glucose, and arabinose). Studies using mutant Mtb strains have shown that the structure of MAs influences the inflammatory potential of these glycolipids. As mutant Mtb strains possess a complex mixture of glycolipids, we analysed the inflammatory potential of single classes of mycolate esters of the Mtb cell wall using 38 different synthetic analogues. Our results show that synthetic trehalose dimycolate (TDM) and trehalose, glucose, and arabinose monomycolates (TMM, GMM, and AraMM) activate bone marrow-derived dendritic cells in terms of the production of pro-inflammatory cytokines (IL-6 and TNF-α) and reactive oxygen species, upregulation of costimulatory molecules, and activation of NLRP3 inflammasome by a mechanism dependent on Mincle. These findings demonstrate that Mincle receptor can also recognise pentose esters and seem to contradict the hypothesis that production of GMM is an escape mechanism used by pathogenic mycobacteria to avoid recognition by the innate immune system. Finally, our experiments indicate that TMM and GMM, as well as TDM, can promote Th1 and Th17 responses in mice in an OVA immunisation model, and that further analysis of their potential as novel adjuvants for subunit vaccines is warranted.
Biochimica et Biophysica Acta | 2017
Grégory Fettweis; Emmanuel Di Valentin; Laurent L'Homme; Cédric Lassence; Franck Dequiedt; Marianne Fillet; Isabelle Coupienne; Jacques Piette
Glioblastomas are the deadliest type of brain cancer and are frequently associated with poor prognosis and a high degree of recurrence despite removal by surgical resection and treatment by chemo- and radio-therapy. Photodynamic therapy (PDT) is a treatment well known to induce mainly necrotic and apoptotic cell death in solid tumors. 5-Aminolevulinic acid (5-ALA)-based PDT was recently shown to sensitize human glioblastoma cells (LN-18) to a RIP3 (Receptor Interacting Protein 3)-dependent cell death which is counter-acted by activation of autophagy. These promising results led us to investigate the pathways involved in cell death and survival mechanisms occurring in glioblastoma following PDT. In the present study, we describe a new TSC2 (Tuberous Sclerosis 2)-dependent survival pathway implicating MK2 (MAPKAPK2) kinase and 14-3-3 proteins which conducts to the activation of a pro-survival autophagy. Moreover, we characterized a new RIP3/TSC2 complex where RIP3 is suggested to promote cell death by targeting TSC2-dependent survival pathway. These results highlight (i) a new role of TSC2 to protect glioblastoma against PDT-induced cell death and (ii) TSC2 and 14-3-3 as new RIP3 partners.
Journal of Virology | 2015
Laura Riva; Marc Thiry; Marielle Lebrun; Laurent L'Homme; Jacques Piette; Catherine Sadzot-Delvaux
ABSTRACT The protein encoded by ORF9 is essential for varicella-zoster virus (VZV) replication. Previous studies documented its presence in the trans-Golgi network and its involvement in secondary envelopment. In this work, we deleted the ORF9p acidic cluster, destroying its interaction with ORF47p, and this resulted in a nuclear accumulation of both proteins. This phenotype results in an accumulation of primary enveloped capsids in the perinuclear space, reflecting a capsid de-envelopment defect.
Journal of Virology | 2018
Laura Riva; Ok-Ryul Song; Jannick Prentoe; François Helle; Laurent L'Homme; Charles-Henry Gattolliat; Alexandre Vandeputte; Lucie Fénéant; Sandrine Belouzard; Thomas Baumert; Tarik Asselah; Jens Bukh; Priscille Brodin; Laurence Cocquerel; Yves Rouillé; Jean Dubuisson
Archive | 2017
Megan Colonval; Grégory Fettweis; Laurent L'Homme; Jacques Piette; Sylvie Legrand
Archive | 2016
Hermann Giresse Tima; J.R. Al Dulayymi; Olivier Denis; P. Lehebel; Klarah Sherzad Baols; Mohsin O. Mohammed; Laurent L'Homme; Mohaned M. Sahb; Georges Potemberg; Sylvie Legrand; R. Lang; Rudi Beyaert; Jacques Piette; Baird; Kris Huygen; Marta Romano
Archive | 2016
Marco Gianfrancesco; Katarzyna Bloch; Jonas Dehairs; Laurent L'Homme; Johan Swinnen; Jacques Piette; André Scheen; Nicolas Paquot; Sylvie Poels-Legrand; Nathalie Esser
Diabetologia | 2016
Marco Gianfrancesco; Jonas Dehairs; Katarzyna Bloch; Laurent L'Homme; Jacques Piette; Johan Swinnen; Nicolas Paquot; Nathalie Esser; Sylvie Legrand