Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bacteroides is increased in an autism cohort and induces autismrelevant behavioral changes in mice in a sex-dependent manner

ABSTRACT: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition which is defined by decreased social communication and the presence of repetitive or stereotypic behaviors. Recent evidence has suggested that the gut-brain axis may be important in neurodevelopment in general and may play a role in ASD in particular. Here, we present a study of the gut microbiome in 96 individuals diagnosed with ASD in Israel, compared to 42 neurotypical individuals. We determined differences in alpha and beta diversity in the microbiome of individuals with ASD and demonstrated that the phylum Bacteroidetes and genus Bacteroides were the most significantly over-represented in individuals with ASD. To understand the possible functional significance of these changes, we treated newborn mice with Bacteroides fragilis at birth. B. fragilis-treated male mice displayed social behavior dysfunction, increased repetitive behaviors and gene expression dysregulation in the prefrontal cortex, while female mice did not display behavioral deficits. These findings suggest that overabundance of Bacteroides, particularly in early life, may have functional consequences for individuals with ASD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE244391 | GEO | 2023/10/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Acetate supplementation rescues social deficits and alters transcriptional regulation in prefrontal cortex of Shank3 deficient mice

Project description:Autism spectrum disorder (ASD) is a heterogenous neurodevelopmental disorder with complex pathophysiology including both genetic and environmental factors. Recent evidence demonstrates the gut microbiome and its resultant metabolome can influence brain and behavior and have been implicated in ASD. To investigate gene by microbiome interactions in a model for genetic risk of ASD, we utilize mutant mice carrying a deletion of the ASD-associated Shank3 gene (Shank3KO). Shank3KO have altered microbiome composition and function at baseline in addition to social deficits. Further depletion of the microbiome with antibiotics exacerbates social deficits in Shank3KO, and results in transcriptional changes in the frontal cortex. Supplementation with the microbial metabolite acetate leads to reversal of social behavioral phenotypes even in mice with a depleted microbiome, and significantly alters transcriptional regulation in the prefrontal cortex. These results suggest a key role for the gut microbiome and the neuroactive metabolite acetate in regulating ASD-like behaviors.

2023-03-02 | GSE225983 | GEO

Human Gut Microbiota from Autism Spectrum Disorder Promote Behavioral Symptoms in Mice

Project description:Autism spectrum disorder (ASD) manifests as alterations in complex human behaviors including social communication and stereotypies. In addition to genetic risks, the gut microbiome differs between typically-developing (TD) and ASD individuals, though it remains unclear whether the microbiome contributes to symptoms. We transplanted gut microbiota from human donors with ASD and TD controls into germ-free mice, and reveal that colonization with ASD microbiota was sufficient to induce hallmark autistic behaviors. The brains of mice colonized with ASD microbiota display alternative splicing of ASD-relevant genes. Microbiome and metabolome profiles of mice harboring human microbiota predict that specific bacterial taxa and their metabolites modulate ASD behaviors. Indeed, treatment of an ASD mouse model with candidate microbial metabolites improves behavioral abnormalities and affects neuronal excitability in the brain. We propose that the gut microbiome modulates behaviors in mice via production of neuroactive metabolites, suggesting that gut-brain connections contribute to the pathophysiology of ASD.

2019-07-04 | MTBLS726 | MetaboLights

MicroRNA biomarkers in blood for Autism spectrum disorder

Project description:Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social communication deficits and repetitive behaviors. MicroRNAs (miRNAs) have been recently recognized as potential biomarkers of ASD as they are dysregulated in various tissues of individuals with ASD. However, it remains unclear whether miRNA expression is altered in individuals with high-functioning ASD. Here, we investigated the miRNA expression profile in peripheral blood from adults with high-functioning ASD, and age and gender-matched healthy controls. Our findings may provide insights regarding the molecular clues for recognizing high-functioning ASD.

2020-05-03 | GSE89596 | GEO

Cytogenetics 2.7M and Cytoscan HD 2.8M Microarrays in autistic families in the Lebanese population

Project description:Autism spectrum disorder (ASD) affects these core domains: ritualistic-repetitive behaviors, impaired social interaction, and deficits in non-verbal communication/language development. Although ASD is heritable, its extreme heterogeneity defies genetic analyses. A number of ASD susceptibility genes have been identified. The Lebanese population is ideal for uncovering recessive genes because of a high rate of shared ancestry, consanguineous marriages, and high number of offspring per family. We recruited 36 ASD families (ASD: 37, unaffected parents: 36, unaffected siblings: 33). Cytogenetics 2.7M Microarrays/CytoScanâ¢ HD arrays allowed mapping of homozygous regions of the genome.

2017-07-24 | E-MTAB-4963 | biostudies-arrayexpress

Effect of metronidazole on microglial gene expression and gut microbiome composition in the 5XFAD mice model of Alzheimer's disease

Project description:The gut microbiota and innate immune system play critical roles in Alzheimer’s disease (AD). Bacteroides is elevated in AD patients and correlates with cerebrospinal fluid levels of Aβ and tau. We found that increased amyloid-β (Aβ) plaques in Bacteroides fragilis treated APP/PS1-21 mice were associated with altered cortical expression Aβ processing genes. B. fragilis suppressed peripheral CD4+ T cell production of GM-CSF and IL-4 and transcriptional changes in microglia related to GM-CSF and IL-4 signaling, phagocytosis, and protein degradation. Furthermore, B. fragilis impaired the microglial uptake of intracranially injected Aβ42, whereas Erysipelotrichaceae strains increased uptake. Depleting murine Bacteroidetes with metronidazole decreased amyloid load in aged 5xFAD mice, increased CD4+ T cell GM-CSF production, and activated microglial pathways related to cytokine signaling, phagocytosis and lysosomal degradation. These data suggest that the gut microbiome may contribute to AD pathogenesis by suppressing peripheral cytokines and microglia phagocytic function, leading to impaired immune-mediated Aβ clearance.

2024-10-12 | GSE215439 | GEO

Effect of Bacteroides fragilis administration on microglia in WT and the APP-PS1 model of Alzheimer's disease [Bfrag]

2024-10-12 | GSE215438 | GEO

Secretome protein enrichment with click sugars (SPECS) analysis on primary neurons cultured from embryos derived from pregnant mice treated with or without valproic acid

Project description:Autism Spectrum Disorder (ASD) is a developmental disorder characterized by impaired social communication and repetitive behaviors. In recent years, a pharmacological mouse model of ASD involving maternal administration of valproic acid (VPA) has become widely used. Newborn pups in this model show an abnormal balance between excitatory and inhibitory (E/I) signaling in neurons and exhibit ASD-like behavior. To elucidate the molecular basis of this model, we analyzed secretome of primary neurons cultured from embryos maternally treated with or without VPA.

2024-10-26 | PXD042099 | JPOST Repository

Expression analysis of Bacteroides fragilis NCTC 9343 delta-ungD1 delta-ungD2 delta-PSH acapsular mutant

Project description:Investigation of whole genome gene expression level changes in a Bacteroides fragilis NCTC 9343 delta-ungD1 delta-ungD2 delta-PSH triple mutant, compared to the wild-type strain. The mutations engineered into this strain render it acapsular. The mutants analyzed in this study are further described in Coyne, M. J., M. Chatzidaki-Livanis, L. C. Paoletti, and L. E. Comstock. 2008. Role of glycan synthesis in colonization of the mammalian gut by the bacterial symbiont Bacteroides fragilis. PNAS 105(35):13098-13103 (PID 18723678). A six chip study using total RNA recovered from three separate wild-type cultures of Bacteroides fragilis NCTC 9343 and three separate cultures of a triple mutant strain, Bacteroides fragilis NCTC 9343 delta-ungD1 delta-ungD2 delta-PSH, in which ungD1 (BF1706), ungD2 (BF2848), and six genes (BF3454 through BF3459) of the PSH capsular polysaccharide locus are truncated or deleted entirely. Each chip measures the expression level of 4,302 genes from Bacteroides fragilis NCTC 9343 and the associated plasmid pBF9343 with fourteen 24-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.

2008-09-02 | E-GEOD-11268 | biostudies-arrayexpress

The interplay between oxidative stress and inflammation supports autistic-related behaviors in Cntnap2 mutant mice

Project description:Autism Spectrum Disorder (ASD) is a highly prevalent neurodevelopmental condition characterized by social communication deficits and repetitive/restricted behaviors. Several studies showed that inflammation may contribute to ASD. Here we used RT-qPCR, RNA sequencing, immunohistochemistry, and flow cytometry to show that pro-inflammatory molecules were increased in the cerebellum and periphery of mice lackingCntnap2(Cntnap2-/-), a robust model of ASD. In parallel, oxidative stress was present in the cerebellum of mutant animals. Systemic treatment with N-acetyl-cysteine (NAC) rescued cerebellar oxidative stress and inflammation as well as motor and social impairments inCntnap2-/-mice. This was accompanied by improved function of microglia cells in NAC-treated mutant animals. Intriguingly, social deficits, cerebellar inflammation and microglia dysfunction were induced by NAC inCntnap2+/+animals. Our findings therefore suggest that the interplay between oxidative stress and inflammation may support ASD-related behaviors in mice.

2024-05-15 | GSE267182 | GEO

Excessive UBE3A dosage impairs fine-tuning of retinoid acid signaling in autism spectrum disorders

Project description:The autism spectrum disorders (ASD) are a collection of disorders with heterogeneous etiology, exhibiting common traits including impaired social interactions and communications, repetitive behaviors. 15q11-q13 copy number variations (CNV) were found in 1-3% of ASD cases; of which the detailed mechanism of the major contributor UBE3A gene acted still remained elusive. Here we identified a key enzyme in RA synthesis, negatively regulated in ubiquitination-dependent mode promoted by UBE3A. Our data provide evidences linking UBE3A hyperactivity with ASD phenotypes, with implications for understanding ASD etiology and providing potential interventions in ASD clinical therapy.

2017-12-28 | GSE93207 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data