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Maternal gut bacteria promote neurodevelopmental abnormalities in mouse offspring
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Journal Article
Maternal gut bacteria promote neurodevelopmental abnormalities in mouse offspring
2017
Overview
Maternal immune activation (MIA)-mediated abnormal behavioural phenotypes require defined gut commensal bacteria for the induction of IL-17-producing T helper 17 cells.
Gut bacteria behind behaviour anomalies
Epidemiological studies have suggested an association between the activation of the maternal immune system (MIA) against viral infections during pregnancy and behavioural abnormalities in the offspring. Earlier studies in mice have demonstrated a role for interleukin-17 (IL-17) in autism spectrum disorder (ASD)-like phenotypes and abnormal cortical development. Here, Gloria Choi, Jun Huh and colleagues provide evidence that MIA-mediated abnormal behavioural phenotypes require defined gut commensal bacteria for the induction of IL-17-producing T helper 17 (T
H
17) cells. In a related study published this week, Gloria Choi, Jun Huh and colleagues identify a specific cortical subregion of the somatosensory cortex as a critical region of dysfunction related to MIA, and show that the presence and size of cortical patches correlate with specific social behaviours.
Maternal immune activation (MIA) contributes to behavioural abnormalities associated with neurodevelopmental disorders in both primate and rodent offspring
1
,
2
,
3
,
4
. In humans, epidemiological studies suggest that exposure of fetuses to maternal inflammation increases the likelihood of developing autism spectrum disorder
5
,
6
,
7
. In pregnant mice, interleukin-17a (IL-17a) produced by T helper 17 (T
H
17) cells (CD4
+
T helper effector cells involved in multiple inflammatory conditions) induces behavioural and cortical abnormalities in the offspring exposed to MIA
8
. However, it is unclear whether other maternal factors are required to promote MIA-associated phenotypes. Moreover, the underlying mechanisms by which MIA leads to T cell activation with increased IL-17a in the maternal circulation are not well understood. Here we show that MIA phenotypes in offspring require maternal intestinal bacteria that promote T
H
17 cell differentiation. Pregnant mice that had been colonized with mouse commensal segmented filamentous bacteria or human commensal bacteria that induce intestinal T
H
17 cells were more likely to produce offspring with MIA-associated abnormalities. We also show that small intestine dendritic cells from pregnant, but not from non-pregnant, females secrete IL-1β, IL-23 and IL-6 and stimulate T cells to produce IL-17a upon exposure to MIA. Overall, our data suggest that defined gut commensal bacteria with a propensity to induce T
H
17 cells may increase the risk of neurodevelopmental disorders in the offspring of pregnant mothers undergoing immune system activation owing to infections or autoinflammatory syndromes.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/51
/ 14
/ 14/34
/ 14/63
/ 38/77
/ 64/60
/ 82/51
/ 96/21
/ 96/31
/ Animals
/ Autism
/ Bacteria
/ Brain
/ Cortex
/ Dendritic Cells - immunology
/ Exposure
/ Female
/ Fetuses
/ Gastrointestinal Microbiome - immunology
/ Humanities and Social Sciences
/ Interleukin-1beta - immunology
/ Intestine, Small - immunology
/ Intestine, Small - microbiology
/ letter
/ Male
/ Mice
/ Microbiota (Symbiotic organisms)
/ Mothers
/ Neurodevelopmental disorders
/ Prenatal Exposure Delayed Effects - immunology
/ Prenatal Exposure Delayed Effects - microbiology
/ Rodents
/ Science
