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<dc:title xml:lang="en">Development of in vivo and in vitro models of acne inversa</dc:title>
<dcterms:alternative xml:lang="fr">Développement de modèles in vivo et in vitro d’acne inversa</dcterms:alternative>
<dc:subject xml:lang="fr">Maladie de Verneuil</dc:subject>
<dc:subject xml:lang="fr">Acne inversa</dc:subject>
<dc:subject xml:lang="fr">Hidradénite suppurée</dc:subject>
<dc:subject xml:lang="fr">Hidrosadénite</dc:subject>
<dc:subject xml:lang="fr">Peau</dc:subject>
<dc:subject xml:lang="fr">Follicule pileux</dc:subject>
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<dc:subject xml:lang="fr">Inflammatoire</dc:subject>
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<dc:subject xml:lang="fr">Épithélium</dc:subject>
<dc:subject xml:lang="fr">Sang</dc:subject>
<dc:subject xml:lang="fr">Peau reconstruite</dc:subject>
<dc:subject xml:lang="fr">Autophagie</dc:subject>
<dc:subject xml:lang="fr">BATMAN</dc:subject>
<dc:subject xml:lang="en">Verneuil's disease</dc:subject>
<dc:subject xml:lang="en">Acne inversa</dc:subject>
<dc:subject xml:lang="en">Hidradenitis suppurativa</dc:subject>
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<dc:subject xml:lang="en">Autophagy</dc:subject>
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<dcterms:abstract xml:lang="fr">L’hidradénite suppurée (HS) est une maladie chronique et récidivante touchant plus de 600 000 personnes en France, bien qu’elle soit sous-diagnostiquée, et découverte en 1839 par le chirurgien français Velpeau. Des lésions incapacitantes sont provoquées par des follicules pileux obstrués qui finissent par s’infecter, conduisant à une inflammation cutanée sévère et douloureuse. La progression de la maladie est propre à chaque individu, certains pouvant voir une rémission intermittente des symptômes ou au contraire une aggravation permanente. Les causes de l’HS sont donc complexes et multifactorielles, et encore aujourd’hui mal comprises. Le diagnostic de l’HS est rendu difficile par une ressemblance avec d’autres maladies cutanées, des praticiens inexpérimentés, et une consultation parfois tardive. De plus, la recherche biomédicale est limitée par une indisponibilité de modèle d’HS, seul le matériel humain, difficile d’accès, pouvant être utilisé. Au sein du consortium européen BATMAN, nous avions l’objectif de la mise en place de modèles pour l’HS, afin d’en faciliter l’étude en laboratoire et ainsi mieux comprendre et combattre la maladie. Utilisant des lignées épithéliales et du matériel primaire humain, nous avons étudié la mise au point de modèles in vitro de peau reconstruite. Nous avons également étudié des modèles murins ciblant l’autophagie dans le follicule, imitant des mutations connues chez certains patients. Enfin, l’analyse cellulaire du sang de patients de l’HS a permis d’identifier plusieurs potentiels marqueurs de la maladie et de sa progression.</dcterms:abstract>
<dcterms:abstract xml:lang="en">Discovered in 1839 by French surgeon Velpeau, hidradenitis suppurativa (HS) is a chronic and relapsing disease affecting more than 40 million people worldwide, although it is an underdiagnosed condition. Debilitating lesions are caused by clogged hair follicles that eventually become infected, leading to severe and painful skin inflammation. The progression of the disease is specific to everyone, some may witness an intermittent remission of symptoms or, instead, experience worsening symptoms. HS causes are therefore complex and multifactorial, and still poorly understood today. HS diagnosis is hindered by a close resemblance to other skin diseases, inexperienced healthcare professionals, and sometimes late medical visits. Moreover, biomedical research is limited by the unavailability of HS models, and only hard-to-come-by human material can be used effectively. Within the European consortium BATMAN, we were tasked with creating HS models to facilitate its study in laboratories, thus better understand and fight the disease. Using epithelial cell lines and human primary material, we studied the generation of in vitro models of reconstructed skin. We also generated mouse models targeting autophagy in the hair follicle, mimicking known patient mutations. Finally, white blood cell analysis of HS patients allowed the identification of several potential markers of the disease and its progression.</dcterms:abstract>
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