La sénescence cellulaire, nouvelle cible ...
Document type :
Article dans une revue scientifique: Article original
PMID :
Title :
La sénescence cellulaire, nouvelle cible des infections virales respiratoires : du virus influenza au SARS-CoV-2
Author(s) :
Sauve, Florent [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Nampoothiri, Sreekala [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Clarke, Sophie [Auteur]
Imperial College London
Fernandois, Daniela [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Ferreira Coêlho, Caio Fernando [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Dewisme, Julie [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Mills, Edouard [Auteur]
Imperial College London
Ternier, Gaetan [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Cotellessa, Ludovica [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Iglesias-Garcia, Cristina [Auteur]
Universidade de Santiago de Compostela [Spain] [USC ]
Mueller-Fielitz, Helge [Auteur]
Universität zu Lübeck = University of Lübeck [Lübeck]
Lebouvier, Thibaud [Auteur]
Perbet, Romain [Auteur]
Florent, Vincent [Auteur]
Baroncini, Marc [Auteur]
Sharif, Ariane [Auteur]
Ereño-Orbea, June [Auteur]
Mercado-Gómez, Maria [Auteur]
Palazon, Asis [Auteur]
Mattot, Virginie [Auteur]
Pasquier, Florence [Auteur]
Catteau-Jonard, Sophie [Auteur]
Martinez-Chantar, Maria [Auteur]
Hrabovszky, Erik [Auteur]
Jourdain, Mercé [Auteur]
Recherche translationnelle sur le diabète - U 1190 [RTD]
Deplanque, Dominique [Auteur]
Centre d'Investigation Clinique - Innovation Technologique de Lille - CIC 1403 - CIC 9301 [CIC Lille]
Morelli, Annamaria [Auteur]
Università degli Studi di Firenze = University of Florence = Université de Florence [UniFI]
Guarnieri, Giulia [Auteur]
Università degli Studi di Firenze = University of Florence = Université de Florence [UniFI]
Storme, Laurent [Auteur]
Hôpital Jeanne de Flandre [Lille]
Robil, Cyril [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Trottein, François [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Nogueiras, Ruben [Auteur]
Schwaninger, Markus [Auteur]
Pigny, Pascal [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Poissy, Julien [Auteur]
Chachlaki, Konstantina [Auteur]
Maurage, Claude-Alain [Auteur]
Giacobini, Paolo [Auteur]
Dhillo, Waljit [Auteur]
Rasika, S. [Auteur]
Prevot, Vincent [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Nampoothiri, Sreekala [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Clarke, Sophie [Auteur]
Imperial College London
Fernandois, Daniela [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Ferreira Coêlho, Caio Fernando [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Dewisme, Julie [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Mills, Edouard [Auteur]
Imperial College London
Ternier, Gaetan [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Cotellessa, Ludovica [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Iglesias-Garcia, Cristina [Auteur]
Universidade de Santiago de Compostela [Spain] [USC ]
Mueller-Fielitz, Helge [Auteur]
Universität zu Lübeck = University of Lübeck [Lübeck]
Lebouvier, Thibaud [Auteur]
Perbet, Romain [Auteur]
Florent, Vincent [Auteur]
Baroncini, Marc [Auteur]
Sharif, Ariane [Auteur]
Ereño-Orbea, June [Auteur]
Mercado-Gómez, Maria [Auteur]
Palazon, Asis [Auteur]
Mattot, Virginie [Auteur]
Pasquier, Florence [Auteur]
Catteau-Jonard, Sophie [Auteur]
Martinez-Chantar, Maria [Auteur]
Hrabovszky, Erik [Auteur]
Jourdain, Mercé [Auteur]
Recherche translationnelle sur le diabète - U 1190 [RTD]
Deplanque, Dominique [Auteur]
Centre d'Investigation Clinique - Innovation Technologique de Lille - CIC 1403 - CIC 9301 [CIC Lille]
Morelli, Annamaria [Auteur]
Università degli Studi di Firenze = University of Florence = Université de Florence [UniFI]
Guarnieri, Giulia [Auteur]
Università degli Studi di Firenze = University of Florence = Université de Florence [UniFI]
Storme, Laurent [Auteur]
Hôpital Jeanne de Flandre [Lille]
Robil, Cyril [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Trottein, François [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Nogueiras, Ruben [Auteur]
Schwaninger, Markus [Auteur]
Pigny, Pascal [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Poissy, Julien [Auteur]
Chachlaki, Konstantina [Auteur]
Maurage, Claude-Alain [Auteur]
Giacobini, Paolo [Auteur]
Dhillo, Waljit [Auteur]
Rasika, S. [Auteur]
Prevot, Vincent [Auteur]
Journal title :
EBioMedicine
Pages :
104784
Publisher :
Elsevier
Publication date :
2023-10
ISSN :
2352-3964
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
BackgroundWe have recently demonstrated a causal link between loss of gonadotropin-releasing hormone (GnRH), the master molecule regulating reproduction, and cognitive deficits during pathological aging, including Down ...
Show more >BackgroundWe have recently demonstrated a causal link between loss of gonadotropin-releasing hormone (GnRH), the master molecule regulating reproduction, and cognitive deficits during pathological aging, including Down syndrome and Alzheimer's disease. Olfactory and cognitive alterations, which persist in some COVID-19 patients, and long-term hypotestosteronaemia in SARS-CoV-2-infected men are also reminiscent of the consequences of deficient GnRH, suggesting that GnRH system neuroinvasion could underlie certain post-COVID symptoms and thus lead to accelerated or exacerbated cognitive decline.MethodsWe explored the hormonal profile of COVID-19 patients and targets of SARS-CoV-2 infection in post-mortem patient brains and human fetal tissue.FindingsWe found that persistent hypotestosteronaemia in some men could indeed be of hypothalamic origin, favouring post-COVID cognitive or neurological symptoms, and that changes in testosterone levels and body weight over time were inversely correlated. Infection of olfactory sensory neurons and multifunctional hypothalamic glia called tanycytes highlighted at least two viable neuroinvasion routes. Furthermore, GnRH neurons themselves were dying in all patient brains studied, dramatically reducing GnRH expression. Human fetal olfactory and vomeronasal epithelia, from which GnRH neurons arise, and fetal GnRH neurons also appeared susceptible to infection.InterpretationPutative GnRH neuron and tanycyte dysfunction following SARS-CoV-2 neuroinvasion could be responsible for serious reproductive, metabolic, and mental health consequences in long-COVID and lead to an increased risk of neurodevelopmental and neurodegenerative pathologies over time in all age groups.Show less >
Show more >BackgroundWe have recently demonstrated a causal link between loss of gonadotropin-releasing hormone (GnRH), the master molecule regulating reproduction, and cognitive deficits during pathological aging, including Down syndrome and Alzheimer's disease. Olfactory and cognitive alterations, which persist in some COVID-19 patients, and long-term hypotestosteronaemia in SARS-CoV-2-infected men are also reminiscent of the consequences of deficient GnRH, suggesting that GnRH system neuroinvasion could underlie certain post-COVID symptoms and thus lead to accelerated or exacerbated cognitive decline.MethodsWe explored the hormonal profile of COVID-19 patients and targets of SARS-CoV-2 infection in post-mortem patient brains and human fetal tissue.FindingsWe found that persistent hypotestosteronaemia in some men could indeed be of hypothalamic origin, favouring post-COVID cognitive or neurological symptoms, and that changes in testosterone levels and body weight over time were inversely correlated. Infection of olfactory sensory neurons and multifunctional hypothalamic glia called tanycytes highlighted at least two viable neuroinvasion routes. Furthermore, GnRH neurons themselves were dying in all patient brains studied, dramatically reducing GnRH expression. Human fetal olfactory and vomeronasal epithelia, from which GnRH neurons arise, and fetal GnRH neurons also appeared susceptible to infection.InterpretationPutative GnRH neuron and tanycyte dysfunction following SARS-CoV-2 neuroinvasion could be responsible for serious reproductive, metabolic, and mental health consequences in long-COVID and lead to an increased risk of neurodevelopmental and neurodegenerative pathologies over time in all age groups.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
ANR Project :
Source :
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