The Effect of Parental Faecal Microbiome Transplantation from Children with Autism Spectrum Disorder on Behavior and Gastrointestinal Manifestations in the Male Offspring of Shank3 Mice

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F25%3A00637567" target="_blank" >RIV/61388963:_____/25:00637567 - isvavai.cz</a>

Výsledek na webu

<a href="https://doi.org/10.3390/ijms26135927" target="_blank" >https://doi.org/10.3390/ijms26135927</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/ijms26135927" target="_blank" >10.3390/ijms26135927</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The Effect of Parental Faecal Microbiome Transplantation from Children with Autism Spectrum Disorder on Behavior and Gastrointestinal Manifestations in the Male Offspring of Shank3 Mice

Popis výsledku v původním jazyce

The increasing incidence of autism spectrum disorder (ASD) increases the urgency of establishing the mechanism of its development for effective prevention and treatment. ASD's etiology includes genetic predisposition and environmental triggers, both of which can play a role in the changed microbiota. Recent research has proved the impact of maternal microbiota on the neurodevelopment of the child. To investigate the co-play of genetic and microbiota factors in ASD development, we performed fecal microbiota transplantation (FMT) from children with ASD to female Shank3b+/- mice and studied the autism-like symptoms in the male Shank3b-/- and wild-type (WT) offspring. WT animals with prenatal exposure to ASD microbiota had delayed neurodevelopment and impaired food intake behavior, but also elevated plasma leptin concentration and body weight. Shank3b-/- mice after FMT ASD exhibited impaired learning and exacerbated anxiety-like behavior in adulthood. Interestingly, FMT ASD improved learning in adolescent Shank3b-/- mice. Prenatal exposure to ASD microbiota decreased the activity of hypocretin neurons of the lateral hypothalamic area in both genotypes. The combination of genetic predisposition and FMT ASD led to an increased colon permeability, evaluated by zonula occludens (ZO1, ZO3) and claudin factors. These results suggest the effect of parental FMT exposure on shaping offspring behavior in Shank3b-/- mice and the potential of microbiota in the modulation of ASD.

Název v anglickém jazyce

The Effect of Parental Faecal Microbiome Transplantation from Children with Autism Spectrum Disorder on Behavior and Gastrointestinal Manifestations in the Male Offspring of Shank3 Mice

Popis výsledku anglicky

The increasing incidence of autism spectrum disorder (ASD) increases the urgency of establishing the mechanism of its development for effective prevention and treatment. ASD's etiology includes genetic predisposition and environmental triggers, both of which can play a role in the changed microbiota. Recent research has proved the impact of maternal microbiota on the neurodevelopment of the child. To investigate the co-play of genetic and microbiota factors in ASD development, we performed fecal microbiota transplantation (FMT) from children with ASD to female Shank3b+/- mice and studied the autism-like symptoms in the male Shank3b-/- and wild-type (WT) offspring. WT animals with prenatal exposure to ASD microbiota had delayed neurodevelopment and impaired food intake behavior, but also elevated plasma leptin concentration and body weight. Shank3b-/- mice after FMT ASD exhibited impaired learning and exacerbated anxiety-like behavior in adulthood. Interestingly, FMT ASD improved learning in adolescent Shank3b-/- mice. Prenatal exposure to ASD microbiota decreased the activity of hypocretin neurons of the lateral hypothalamic area in both genotypes. The combination of genetic predisposition and FMT ASD led to an increased colon permeability, evaluated by zonula occludens (ZO1, ZO3) and claudin factors. These results suggest the effect of parental FMT exposure on shaping offspring behavior in Shank3b-/- mice and the potential of microbiota in the modulation of ASD.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

International Journal of Molecular Sciences

ISSN

1661-6596

e-ISSN

1422-0067

Svazek periodika

26

Číslo periodika v rámci svazku

13

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

27

Strana od-do

5927

Kód UT WoS článku

001526386200001

EID výsledku v databázi Scopus

2-s2.0-105010298227