Depicting the composition of gut microbiota in children with tic disorders: an exploratory study / W. XI in Journal of Child Psychology and Psychiatry, 62-10 (October 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1246-1254 Titre : Depicting the composition of gut microbiota in children with tic disorders: an exploratory study Type de document : Texte imprimé et/ou numérique Auteurs : W. XI, Auteur ; X. GAO, Auteur ; H. ZHAO, Auteur ; X. LUO, Auteur ; J. LI, Auteur ; X. TAN, Auteur ; L. WANG, Auteur ; J. B. ZHAO, Auteur ; J. WANG, Auteur ; G. YANG, Auteur ; L. Y. LIU, Auteur ; Y. Y. WANG, Auteur ; L. PENG, Auteur ; L. P. ZOU, Auteur ; Y. YANG, Auteur Article en page(s) : p.1246-1254 Langues : Anglais (eng) Mots-clés : Bacteroides  Child  Gastrointestinal Microbiome  Humans  Prevotella  Ruminococcus  Streptococcus  Tic Disorders  dopamine receptor antagonists  gut microbiota  metabolic pathways  metagenomics Index. décimale : PER Périodiques Résumé : BACKGROUND: Symptom improvement in children with tic disorder (TD) following fecal microbiota transplantation led us to investigate the gut microbiota in TD. This exploratory study aims to depict the gut microbial profile in patients with TD and explore the impact of dopamine receptor antagonist (DRA) drugs on the composition and metabolic function of the gut microbiota. METHODS: The gut microbiota were profiled in fecal samples of 49 children with TD and 50 matched healthy controls (HC) using shotgun metagenomic sequencing. A random forest (RF) model was constructed using the gut bacterial species to distinguish TD from HC. Associations between clinical metadata and microbial abundance or function were analyzed using MaAsLin2 and Spearman correlation. RESULTS: The gut microbiota in children with TD was featured by higher abundances of Bacteroides plebeius and Ruminococcus lactaris (a potential pro-inflammatory taxon) and lower abundances of Prevotella stercorea and Streptococcus lutetiensis compared to HC. The constructed RF model accurately distinguished TD from HC based on the gut microbiota profile, resulting in an AUC of 0.884. Significant correlations were observed between tic symptom severity and the abundances of multiple bacterial species and gut microbiota metabolic functions. Multivariate analysis identified an upregulation of 4-aminobutanoate (GABA) degradation in the gut microbiota associated with TD status. The gut microbiota of DRA-treated TD children showed a distinct gut microbiota compared to the treatment-naïve group, represented by an increase in some potential enteric pathogens such as Escherichia coli, a decline in several species including Akkermansia muciniphila, and alterations in various metabolic functions. CONCLUSIONS: Bacterial species promoting inflammatory responses and those modulating neurotransmitters such as GABA may be involved in the pathogenesis of TD. The use of DRA drugs is likely to induce overgrowth of some enteric pathogens and alter the gut microbiota metabolism. En ligne : http://dx.doi.org/10.1111/jcpp.13409 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 [article] Depicting the composition of gut microbiota in children with tic disorders: an exploratory study [Texte imprimé et/ou numérique] / W. XI, Auteur ; X. GAO, Auteur ; H. ZHAO, Auteur ; X. LUO, Auteur ; J. LI, Auteur ; X. TAN, Auteur ; L. WANG, Auteur ; J. B. ZHAO, Auteur ; J. WANG, Auteur ; G. YANG, Auteur ; L. Y. LIU, Auteur ; Y. Y. WANG, Auteur ; L. PENG, Auteur ; L. P. ZOU, Auteur ; Y. YANG, Auteur . - p.1246-1254. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1246-1254 Mots-clés : Bacteroides  Child  Gastrointestinal Microbiome  Humans  Prevotella  Ruminococcus  Streptococcus  Tic Disorders  dopamine receptor antagonists  gut microbiota  metabolic pathways  metagenomics Index. décimale : PER Périodiques Résumé : BACKGROUND: Symptom improvement in children with tic disorder (TD) following fecal microbiota transplantation led us to investigate the gut microbiota in TD. This exploratory study aims to depict the gut microbial profile in patients with TD and explore the impact of dopamine receptor antagonist (DRA) drugs on the composition and metabolic function of the gut microbiota. METHODS: The gut microbiota were profiled in fecal samples of 49 children with TD and 50 matched healthy controls (HC) using shotgun metagenomic sequencing. A random forest (RF) model was constructed using the gut bacterial species to distinguish TD from HC. Associations between clinical metadata and microbial abundance or function were analyzed using MaAsLin2 and Spearman correlation. RESULTS: The gut microbiota in children with TD was featured by higher abundances of Bacteroides plebeius and Ruminococcus lactaris (a potential pro-inflammatory taxon) and lower abundances of Prevotella stercorea and Streptococcus lutetiensis compared to HC. The constructed RF model accurately distinguished TD from HC based on the gut microbiota profile, resulting in an AUC of 0.884. Significant correlations were observed between tic symptom severity and the abundances of multiple bacterial species and gut microbiota metabolic functions. Multivariate analysis identified an upregulation of 4-aminobutanoate (GABA) degradation in the gut microbiota associated with TD status. The gut microbiota of DRA-treated TD children showed a distinct gut microbiota compared to the treatment-naïve group, represented by an increase in some potential enteric pathogens such as Escherichia coli, a decline in several species including Akkermansia muciniphila, and alterations in various metabolic functions. CONCLUSIONS: Bacterial species promoting inflammatory responses and those modulating neurotransmitters such as GABA may be involved in the pathogenesis of TD. The use of DRA drugs is likely to induce overgrowth of some enteric pathogens and alter the gut microbiota metabolism. En ligne : http://dx.doi.org/10.1111/jcpp.13409 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456

Development of neurodevelopmental disorders: a regulatory mechanism involving bromodomain-containing proteins / J. LI in Journal of Neurodevelopmental Disorders, 5-1 (December 2013)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 5-1 (December 2013) . - p.4 Titre : Development of neurodevelopmental disorders: a regulatory mechanism involving bromodomain-containing proteins Type de document : Texte imprimé et/ou numérique Auteurs : J. LI, Auteur ; G. ZHAO, Auteur ; X. GAO, Auteur Article en page(s) : p.4 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Neurodevelopmental disorders are classified as diseases that cause abnormal functions of the brain or central nervous system. Children with neurodevelopmental disorders show impaired language and speech abilities, learning and memory damage, and poor motor skills. However, we still know very little about the molecular etiology of these disorders. Recent evidence implicates the bromodomain-containing proteins (BCPs) in the initiation and development of neurodevelopmental disorders. BCPs have a particular domain, the bromodomain (Brd), which was originally identified as specifically binding acetyl-lysine residues at the N-terminus of histone proteins in vitro and in vivo. Other domains of BCPs are responsible for binding partner proteins to form regulatory complexes. Once these complexes are assembled, BCPs alter chromosomal states and regulate gene expression. Some BCP complexes bind nucleosomes, are involved in basal transcription regulation, and influence the transcription of many genes. However, most BCPs are involved in targeting. For example, some BCPs function as a recruitment platform or scaffold through their Brds-binding targeting sites. Others are recruited to form a complex to bind the targeting sites of their partners. The regulation mediated by these proteins is especially critical during normal and abnormal development. Mutant BCPs or dysfunctional BCP-containing complexes are implicated in the initiation and development of neurodevelopmental disorders. However, the pathogenic molecular mechanisms are not fully understood. In this review, we focus on the roles of regulatory BCPs associated with neurodevelopmental disorders, including mental retardation, Fragile X syndrome (FRX), Williams syndrome (WS), Rett syndrome and Rubinstein-Taybi syndrome (RTS). A better understanding of the molecular pathogenesis, based upon the roles of BCPs, will lead to screening of targets for the treatment of neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1186/1866-1955-5-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=345 [article] Development of neurodevelopmental disorders: a regulatory mechanism involving bromodomain-containing proteins [Texte imprimé et/ou numérique] / J. LI, Auteur ; G. ZHAO, Auteur ; X. GAO, Auteur . - p.4. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 5-1 (December 2013) . - p.4 Index. décimale : PER Périodiques Résumé : Neurodevelopmental disorders are classified as diseases that cause abnormal functions of the brain or central nervous system. Children with neurodevelopmental disorders show impaired language and speech abilities, learning and memory damage, and poor motor skills. However, we still know very little about the molecular etiology of these disorders. Recent evidence implicates the bromodomain-containing proteins (BCPs) in the initiation and development of neurodevelopmental disorders. BCPs have a particular domain, the bromodomain (Brd), which was originally identified as specifically binding acetyl-lysine residues at the N-terminus of histone proteins in vitro and in vivo. Other domains of BCPs are responsible for binding partner proteins to form regulatory complexes. Once these complexes are assembled, BCPs alter chromosomal states and regulate gene expression. Some BCP complexes bind nucleosomes, are involved in basal transcription regulation, and influence the transcription of many genes. However, most BCPs are involved in targeting. For example, some BCPs function as a recruitment platform or scaffold through their Brds-binding targeting sites. Others are recruited to form a complex to bind the targeting sites of their partners. The regulation mediated by these proteins is especially critical during normal and abnormal development. Mutant BCPs or dysfunctional BCP-containing complexes are implicated in the initiation and development of neurodevelopmental disorders. However, the pathogenic molecular mechanisms are not fully understood. In this review, we focus on the roles of regulatory BCPs associated with neurodevelopmental disorders, including mental retardation, Fragile X syndrome (FRX), Williams syndrome (WS), Rett syndrome and Rubinstein-Taybi syndrome (RTS). A better understanding of the molecular pathogenesis, based upon the roles of BCPs, will lead to screening of targets for the treatment of neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1186/1866-1955-5-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=345

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