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Maternal gut bacteria drive intestinal inflammation in offspring with neurodevelopmental disorders by altering the chromatin landscape of CD4+ T cells

Authors
 Eunha Kim  ;  Donggi Paik  ;  Ricardo N Ramirez  ;  Delaney G Biggs  ;  Youngjun Park  ;  Ho-Keun Kwon  ;  Gloria B Choi  ;  Jun R Huh 
Citation
 IMMUNITY, Vol.55(1) : 145-158, 2022-01 
Journal Title
IMMUNITY
ISSN
 1074-7613 
Issue Date
2022-01
MeSH
Animals ; Autism Spectrum Disorder / immunology* ; Autism Spectrum Disorder / microbiology ; CD4-Positive T-Lymphocytes / immunology* ; Child ; Chromatin / metabolism* ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Female ; Gastrointestinal Microbiome / immunology* ; Humans ; Immunization ; Inflammation / immunology* ; Inflammation / microbiology ; Interleukin-17 / metabolism* ; Intestines / immunology* ; Mice ; Neurodevelopmental Disorders / immunology* ; Neurodevelopmental Disorders / microbiology ; Pregnancy ; Prenatal Exposure Delayed Effects / immunology* ; Prenatal Exposure Delayed Effects / microbiology
Keywords
Citrobacter ; autism spectrum disorder ; colitis ; gut microbiota ; inflammatory bowel diseases ; interleukin-17A ; maternal immune activation ; neurodevelopmental disorders ; pregnancy
Abstract
Children with autism spectrum disorders often display dysregulated immune responses and related gastrointestinal symptoms. However, the underlying mechanisms leading to the development of both phenotypes have not been elucidated. Here, we show that mouse offspring exhibiting autism-like phenotypes due to prenatal exposure to maternal inflammation were more susceptible to developing intestinal inflammation following challenges later in life. In contrast to its prenatal role in neurodevelopmental phenotypes, interleukin-17A (IL-17A) generated immune-primed phenotypes in offspring through changes in the maternal gut microbiota that led to postnatal alterations in the chromatin landscape of naive CD4+ T cells. The transfer of stool samples from pregnant mice with enhanced IL-17A responses into germ-free dams produced immune-primed phenotypes in offspring. Our study provides mechanistic insights into why children exposed to heightened inflammation in the womb might have an increased risk of developing inflammatory diseases in addition to neurodevelopmental disorders.
Files in This Item:
T202204406.pdf Download
DOI
10.1016/j.immuni.2021.11.005
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Kwon, Ho-Keun(권호근) ORCID logo https://orcid.org/0000-0003-3175-0376
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/192734
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