The Maternal Microbiome and Autism

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Autism spectrum disorders (ASD) are a series of development disorders which include autistic disorder, Rett’s disorder, childhood disintegrative disorder, and Asperger’s syndrome. Autism spectrum disorders are classically characterized by, among others, severe and pervasive impairment in several areas of social and behavioural development (5). Recently, numerous basic science studies in mice and epidemiological studies in humans have revealed a link between Maternal Immune Activation (MIA) and ASD phenotypes (2-4, 6).

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Furthermore, instances of MIA leading to ASD like phenotypes appear to be primarily linked to immune activation in the first 2 trimesters (7). Herein, we will review several recent studies that begin to elucidate the mechanism linking MIA and ASD as well as the key role played by the maternal micorbiota in driving these pathways.

Hsiao et al. 2013, demonstrates GI barrier defects and microbiota alterations in the MIA model displaying offpsing with ASD-like phenotypes. Parrallelling epidemiological studies in humans that showed increased instances of IBD and other GI disorders were highly prevelant in ASD individuals (9). Investigators demonstrated that adult MIA offspring exhibited a number of similar GI defects, notably increased gut permeability as demonstrated by the translocation of dextran across the intestinal epithelium (8). The disbiosis of gut microbiota was also described in ASD individuals, and while a well defined ASD-assocaiated microbiota has not been established, rigorous examination of the composition of the ASD-associated microbiota revealed that while overall abundance of identified bacteria did not change, the alterations in the specific operational taxonomic units of both Clostridia and Bacteroidial were significant. Introduction of B. fragilis, which had been previously shown to emeleriate colitis (15) was able to correct the intestinal permeability in MIA offspring. In addition, administration of B. fragilis restored MIA-associated increases in IL-6, which has been previoulsy shown to be increased in MIA mothers and offspring (6, 10). Treatment with B. fragilis not only decreased the GI defects in MIA offspring, it also acted to return the microbiota toxonomy toward a more “normal” composition, reducing the disproportionate ratios found in MIA offspring. In addition to restoring the normal microbiota composition B. fragilis treatment also reduced ASD-like behavioural abnormalities. Suggesting a link between the microbiome and CNS that is still largely unexplored.

Next we examine the effect of the maternal microbiota on early postnatal immune system development as described by de Aguero et al.. Here investigators used gestation-only colonization and germ-free delivery to ensure that any change in neonatal immune composition was limited to encounters with the maternal microbiota only during gestation. At 14 days post-birth it was shown that elevated numbers of early post-natal intestinal innate leukocytes, specifically the NKp46+ROR?t+ ILC3 subpopulaiton, as well as intestinal F4/80+CD11c+ mononulcear cells (iMNC) were present in pups born to gestation-only colonized dams compared to germ-free controls. Counter to the innate leukocyte alterations seen in the germ-free animals,

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