📇 Rhumatologue · BOULOGNE BILLANCOURT CEDEX · (92) · Hospitalier

M MARCEL BONAY

Pourquoi vous devez consulter ce praticien

5 raisons identifiées

Plateau technique de référence
Assistance publique – Hôpitaux de Paris (APHP) — équipements et expertise pointus pour les cas complexes
Auteur de référence en rhumatologie
45 articles scientifiques publiés — un praticien à la pointe de la recherche
Encadrant universitaire
Forme la prochaine génération de rhumatologues (6 thèses dirigées)
Expérience confirmée
30 ans d'exercice en rhumatologie — recul clinique solide
Délais de RDV courts dans la région
136 rhumatos / 100 000 hab. — département bien doté

Rhumatologue

📍 BOULOGNE BILLANCOURT CEDEX (92)HospitalierRPPS 10001065407

EnseignementExpérience confirmée

30ans d'exercice (thèse 1996)

📊 Reconnaissance scientifique : 27/100📝 121 articles publiés🇫🇷 Publications académiques françaises (8)🎓 6 thèses dirigées

Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.

Top publications · les plus citées

Nuclear factor erythroid 2-related factor 2 nuclear translocation induces myofibroblastic dedifferentiation in idiopathic pulmonary fibrosis

Antioxidants & redox signaling · 2013

📚 124 citations🎯 RCR 4.10Top 10% NIH🔓 Open Access

Lire l'abstract Crossref ↓

Aims: Oxidants have been implicated in the pathophysiology of idiopathic pulmonary fibrosis (IPF), especially in myofibroblastic differentiation. We aimed at testing the hypothesis that nuclear factor erythroid 2-related factor 2 (Nrf2), the main regulator of endogenous antioxidant enzymes, is involved in fibrogenesis via myofibroblastic differentiation. Fibroblasts were cultured from the lungs of eight controls and eight IPF patients. Oxidants–antioxidants balance, nuclear Nrf2 expression, and fibroblast phenotype (α-smooth muscle actin and collagen I expression, proliferation, migration, and contraction) were studied under basal conditions and after Nrf2 knockdown or activation by Nrf2 or Keap1 siRNA transfection. The effects of sulforaphane (SFN), an Nrf2 activator, on the fibroblast phenotype were tested under basal and pro-fibrosis conditions (transforming growth factor β [TGF-β]). Results: Decreased Nrf2 expression was associated with a myofibroblast phenotype in IPF compared with control fibroblasts. Nrf2 knockdown induced oxidative stress and myofibroblastic differentiation in control fibroblasts. Conversely, Nrf2 activation increased antioxidant defences and myofibroblastic dedifferentation in IPF fibroblasts. SFN treatment decreased oxidants, and induced Nrf2 expression, antioxidants, and myofibroblastic dedifferentiation in IPF fibroblasts. SFN inhibited TGF-β profibrotic deleterious effects in IPF and control fibroblasts and restored antioxidant defences. Nrf2 knockdown abolished SFN antifibrosis effects, suggesting that they were Nrf2 mediated. Innovation and Conclusion: Our findings confirm that decreased nuclear Nrf2 plays a role in myofibroblastic differentiation and that SFN induces human pulmonary fibroblast dedifferentiation in vitro via Nrf2 activation. Thus, Nrf2 could be a novel therapeutic target in IPF. Antioxid. Redox Signal. 18, 66–79.

Alpha/beta interferon impairs the ability of human macrophages to control growth of Mycobacterium bovis BCG

Infection and immunity · 2002

📚 56 citations🔓 Open Access

Lire l'abstract Crossref ↓

ABSTRACTAdministration of alpha/beta interferon (IFN-α/β) to mice infected withMycobacterium tuberculosishas been shown to increase mycobacterial growth. Because IFN-α/β has direct pleiotropic effects on the differentiation and functional activities of macrophages, we evaluated the effect of IFN-α/β on mycobacterial growth in human monocytes/macrophages in vitro. Monocytes cultured at optimal cell density could control the growth ofM. bovisBCG, as assessed both by measurement of luciferase activity expressed by a mycobacterial reporter strain and by counting of CFU. In contrast, unrestrained mycobacterial growth was observed when monocytes were treated with alpha interferon (IFN-α) 3 days prior to or concomitant with infection. This striking loss of mycobacteriostatic activity was observed with IFN-α and IFN-β and was induced in both freshly isolated monocytes and culture-derived macrophages. Pretreatment of monocytes with IFN-α modified cellular morphology and reduced viability following culture, but neither was observed for culture-derived macrophages, indicating that the effects of IFN-α on mycobacteriostatic activity and cell differentiation and death could be dissociated. These results are compatible with the possibility that the secretion of IFN-α/β could directly promote mycobacterial growth in patients harboring these organisms.

Repeated nitrogen dioxide exposures and eosinophilic airway inflammation in asthmatics: a randomized crossover study

Environmental health perspectives · 2014

📚 45 citations🎯 RCR 1.50🩺 Clinique🔓 Open Access

Cookies & analyse de trafic

M MARCEL BONAY

Pourquoi vous devez consulter ce praticien

Thèses universitaires

Direction de thèses

Activité de recherche & publications

Publications académiques en France

Lieu de consultation

Tarifs & secteur de conventionnement

Prendre rendez-vous & contact

Top publications · les plus citées

Publications scientifiques (45) — classées par pathologie

Transversal36

Santé mentale / fatigue3

Pharmacovigilance2

Case report / série1

Économie santé1

Essai clinique1

Sjögren1

Vraie vie / RWE1

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