Experience

IPMC CNRS - University Nice Sophia Antipolis

• France
• Biotechnology Research
• 1 - 100 Employee

• Chercheure postdoctoral

  • Nov 2022 - Present

  Chronic pain is a major public health problem, resulting in disability, medical costs, psychological distress and deterioration in quality of life. However, available analgesics often have limited efficacy and significant side effects or abuse risk. To define new therapeutical strategies, there is a real need to better understand chronic pain pathophysiology, with identification of both triggering factors and new molecular targets. ASICs (Acid-Sensing Ion Channels) are cationic excitatory ion channels that are emerging as important new players in the field of pain. They are expressed in the whole pain neuraxis, both in peripheral sensory neurons including nociceptors, as well as in central neurons of the spinal cord and the brain. The main objective of my postdoctoral research project is to study the role of endogenous lipids targeting ASIC channels in chronic pain. It is based on both electrophysiological recordings of spinal cord neurons, which gives direct information about pain sensitization mechanisms leading to chronic pain, and on pharmacological, genetic and behavioral approaches in models of chronic pain induced by ASIC-activating lipids. At the end, this project could potentially provide new data to support the inhibition of ASIC channels as a potential therapeutic approach in painful disorders. Show less



Inserm NeuroDol UMR 1107

• Clermont-Ferrand, Auvergne-Rhône-Alpes, France

• Chercheure postdoctoral

  • Apr 2022 - Nov 2022



INSERM

• France
• Research Services
• 700 & Above Employee

• Ph.D Student

  • Oct 2018 - Apr 2022

  Disturbances of brain-gut-microbiota axis are the focus of many studies to develop new treatments for chronic intestinal pathologies such as irritable bowel syndrome (IBS). In some cases, after a gastrointestinal Enterobacteriaceae infection, despite pathogen elimination, transit disorders and chronic abdominal pain persist and can lead to the development of anxiety and depression symptoms. This is referred to post-infectious IBS (PI-IBS). We have shown that the mouse model of C. rodentium infection developed, during the post-infectious period, a persistent colonic hypersensitivity (CHS), anxiety-related behavior as well as cognitive-related alterations, associated with a dysbiosis, a low-grade inflammation and an increased intestinal permeability demonstrating that it is a relevant model to investigate physiopathological mechanisms of PI-IBS. Trytophan metabolism is altered with an indole pathway downregulation and AhR activity as well as a decrease of tryptophol production. Our results suggest that targeting AhR/IL-22 signaling pathway improves the PI-IBS symptoms by acting on the intestinal epithelial barrier integrity and microbiota-derived Trp metabolites. Metabolomics studies were expanded to identify infection-induced functional disturbances of fecal microbiota. This work allowed to clarify pathophysiology associated with PI-IBS and to identify new potential therapeutic targets such as AhR/IL-22 pathway. In addition, role of others infections on host cognitive and emotional behaviors was studied in two animal models. A chronic parasitic infection with Blastocystis in rats was used to mimic IBS, as well as a chronic infection with colibactin-producing Escherichia coli (CoPEC), another Enterobacteria associated with colorectal cancer (CRC). Show less



Institut Cochin

• Région de Paris, France

• Stagiaire

  • May 2017 - Jul 2017

  Recherche fondamentale Sujet : Contrôle de la division de l'hépatocyte stéatosique - Implication de la kinase ATR Responsable : Pr Chantal DESDOUETS & Romain DONNE Résumé : Steatosis is part of a wide range of liver damages, called Non-Alcoholic Fatty Liver Disease (NAFLD), able to lead to an inflammatory state (Non-Alcoholic Steatohepatitis – NASH). This state can guide to the appearance of a cirrhosis and finally to a hepatocellular carcinoma (HCC). By using mice models reproduising the NAFLD/NASH sequence, the laboratory highlighted that exists an hepatocellular ploidy alteration, and genesis of mononuclear polyploids hepatocytes (4n, ≥8n). These appear wihtout mitosis after cell cycles, in response to the activation of the DNA Damage Response (DDR) (ATR/p53/p21), induce by DNA alterations. Many studies have clearly demonstrated that a replication stress can lead to carcinogenesis after chromosomic instability setting up. This polyploid share genesis could protect this tissu by preventing unstables cells proliferation ; especially as ATR gene is found mutated in 5% of human HCC. Initial results shows in a new mouse model (High Fat High Sucrose HFHS) reproduising human pathology NAFLD/NASH, the arrangement of a replication stress. However, ATR leak, create by CRISPR/Cas9 technique, in a NAFLD context, does not look to affect the DDR placing, despite the presence of DNA double-strand breakage. Show less



Laboratoire M2iSH

• Région de Clermont-Ferrand, France

• Stagiaire

  • Apr 2015 - Jun 2015

  Recherche fondamentale Sujet : Etude de la régulation de la synthèse du flagelle par le gène flgM et implication dans la virulence des Escherichia coli adhérents et invasifs Responsable : Mathilde BONNET et Gwladys SEVRIN Résumé : AIEC strains (adherent-iunvasive Escherichia coli) isolated from ideal lesions of Crohn's disease patients are flagellated bacteria able to invade intestinal epithelial cells and to survive intro macrophages. Flagella are required for virulence. non-flagellated AIEC mutants show a reduced ability to invade intestinal epithelial cells. Flagellin, major bacterial flagellum protein, is also recognized by innate immune receptors leading to production of pro-inflammatory cytokines. We hypothesized that efficient modulation of flagellin expression is required for mucosa colonization and in vivo persistence, and allows AIEC to evade innate immune detection. To test this hypothesis, we constructed AIEC LF82 deficient in flgM. This gene encodes a negative regulator of flagellar synthesis. Deletion of flgM impacts type 1 pili and flagella expressions. This is associated with an increased secretion of flagellin in the culture supernatant of the mutant. this study demonstrates that loss of this regulation factor leads to decrease in vitro pathogenicity and to increase pro-inflammatory cytokines release in an infected mouse model. Show less