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  • HOME
  • About
    • DIRECTION
  • Research
    • teams >
      • TEAM 1 PATHOPHYSIOLOGY OF THE INTESTINAL EPITHELIUM
      • ​TEAM 2 PATHOGENESIS AND COMMENSALISM OF ENTEROBACTERIA
      • TEAM 3 INTESTINAL NEURO-IMMUNE INTERACTIONS
      • TEAM 4 IRON METABOLISM: FROM REGULATION TO THERAPY
      • TEAM 5 ERYTHROFERRONE AND IRON HOMEOSTASIS
      • TEAM6 ENVIRONMENT & INTESTINAL EPITHELIUM INTERACTIONS -EINSTEIN-
    • Core facilities >
      • DIGESTIVE MODELS
      • ORGANOIDS
    • Publications >
      • Help for scientific writing
  • EDUCATION
    • MASTER
    • THESIS >
      • THESIS TOPICS PROPOSALS
      • THESIS DEFENSES
  • JOBS
    • JOB OFFERS >
      • GROUP LEADER
    • PREPARATION FOR COMPETITION
  • Events
    • IRSD Retreat >
      • 2016
      • 2017
    • Progress Reports
    • IRSD seminars
  • SERVICES
  • Highlights
  • Pictures
  • Contacts
    • Contact IRSD
    • Contact team
    • Contact Core Facilities
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Núria Solà

DOCTORANTE

PhD student

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00 33 (0)5 62 74 45 23
EQUIPE 1 : PATHOPHYSIOLOGIE DE L’EPITHELIUM INTESTINAL
TEAM 1 : PATHOPHYSIOLOGY OF THE INTESTINAL EPITHELIUM
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Mini CV

  • 2015- actual job: PhD candidate at IRSD
  • 2014 Master in Biomedical Science at Universitat Pompeu Fabra, Barcelona. 6 months internship at Hôpital Bichat, department of Physiopathologie et Épidémiologie de l'Insuffisance Respiratoire
  • 2013 Bachelor in Biomedical Science at Universitat de Barcelona, Barcelona. 10 months internship at Nederlands Kanker Instituut, Amsterdam. Department of Cell Biology. 

expertise

  • Cell culture
  • Protease quantification (trypsin-Like activity cysteine-like activity)
  • Permeability test (Dextran-FITC)
  • Western blotting
  • Gene expression (qPCR)
  • ELISA ABP-prove active enzyme. 

Recherche/projet  research/project

Crosstalk between intestinal ephitelial proteolytic activity and inflammatory bowel diseases
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Crohn’s disease (CD) and ulcerative colitis (UC), the two main subtypes of inflammatory bowel disease (IBD), are chronic relapsing inflammatory disorders of the gastrointestinal tract. Patients suffer from relapsing flares with diarrhoea, abdominal pain and rectal bleeding. To date, the molecular mechanisms of IBD are poorly understood. Nevertheless, many data suggest that inflammatory lesions could be driven by environmental stimuli, inducing an immune dysfunction in genetically predisposed individuals. Since the discovery of NOD2 in 2001, genetic studies have reported more than 170 IBD susceptibility loci.. The strongest associations have highlighted three main pathways involved in IBD: bacterial sensing (NOD2, CD), autophagy (ATG16L1 and IRGM, CD) and the endoplasmic reticulum (ER) stress (XBP1, UC).
Proteases play a key role in the digestion but also in the homeostatic maintenance of the intestinal barrier. Studies from our lab have evidenced excessive proteolytic activity in the context of IBD, associated with a decreased expression of protease inhibitors in the colonic mucosa.
We aim to  study the relationship between the proteolytic activity from intestinal epithelium and the three pathways involved in IBD  (NOD2, autophagy and ER stress)
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INSERM IRSD U1220 , CHU PURPAN PLACE DU DOCTEUR BAYLAC, 
​CS 60039 31024, TOULOUSE CEDEX 3  
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