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2017 ; 10
(1
): 14
Nephropedia Template TP
gab.com Text
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Modeling environmental risk factors of autism in mice induces IBD-related gut
microbial dysbiosis and hyperserotonemia
#MMPMID28427452
Lim JS
; Lim MY
; Choi Y
; Ko G
Mol Brain
2017[Apr]; 10
(1
): 14
PMID28427452
show ga
Autism spectrum disorder (ASD) is a range of neurodevelopmental conditions that
are sharply increasing in prevalence worldwide. Intriguingly, ASD is often
accompanied by an array of systemic aberrations including (1) increased
serotonin, (2) various modes of gastrointestinal disorders, and (3) inflammatory
bowel disease (IBD), albeit the underlying cause for such comorbidities remains
uncertain. Also, accumulating number of studies report that the gut microbial
composition is significantly altered in children with ASD or patients with IBD.
Surprisingly, when we analyzed the gut microbiota of poly I:C and VPA-induced
mouse models of ASD, we found a distinct pattern of microbial dysbiosis that
highly recapitulated those reported in clinical cases of ASD and IBD. Moreover,
we report that such microbial dysbiosis led to notable perturbations in microbial
metabolic pathways that are known to negatively affect the host, especially with
regards to the pathogenesis of ASD and IBD. Lastly, we found that serum level of
serotonin is significantly increased in both poly I:C and VPA mice, and that it
correlates with increases of a bacterial genus and a metabolic pathway that are
implicated in stimulation of host serotonin production. Our results using animal
model identify prenatal environmental risk factors of autism as possible
causative agents of IBD-related gut microbial dysbiosis in ASD, and suggest a
multifaceted role of gut microbiota in the systemic pathogenesis of ASD and
hyperserotonemia.