Gut Microbiota Features in Young Children With Autism Spectrum Disorders Original paper

What was studied?

This study investigated gut microbiota features in young children with autism spectrum disorder (ASD), focusing on microbial composition and fecal short-chain fatty acids (SCFAs). The authors aimed to identify age-specific microbial signatures—an important goal because early childhood represents a crucial neurodevelopmental window. To support precision, the study examined microbiome profiles using 16S rRNA sequencing, species-level assignments, KEGG-based functional predictions, and fecal measurements of butyrate and propionate. This work directly contributes to understanding whether gut microbiota shifts in ASD reflect disruptions in normal colonization patterns, including changes in keystone microbes such as Bifidobacterium longum and Faecalibacterium prausnitzii. These findings help contextualize the broader relationship between ASD and the gut–brain–microbiome axis.

Who was studied?

The study enrolled 11 children aged 2–4 years with newly diagnosed ASD and 14 age-matched neurotypical controls. Participants shared similar dietary habits, lived in an urban setting, and were screened to exclude confounders such as recent antibiotic exposure, metabolic disease, or food intolerances. ASD diagnoses were confirmed through DSM-5 criteria and validated with ADOS-2 and ADI-R. Within the ASD group, severity levels ranged from requiring support to requiring very substantial support. This tightly restricted age band minimizes variability from microbiome maturation differences and enhances detection of ASD-related microbial patterns.

Most important findings

The gut microbiota of ASD children showed distinct taxonomic, functional, and metabolite-level alterations. At the phylum level, ASD participants had increased Bacteroidetes and Proteobacteria, with reduced Actinobacteria. Species-level shifts were particularly notable: B. longum, normally a dominant early-life colonizer supporting gut barrier function and neuroactive metabolite production, was markedly depleted. Conversely, F. prausnitzii, a butyrate-producing late colonizer usually increasing later in childhood, was significantly enriched. Droplet digital PCR confirmed elevated F. prausnitzii copies.

The study identified 91 discriminatory OTUs, including expansions of Bacteroides vulgatus, Bacteroides uniformis, and mucin-degrading Ruminococcus torques. These shifts corresponded to functional differences: KEGG pathway prediction revealed enrichment of butyrate-production genes, including phosphate butyryltransferase and acetate CoA-transferase. Fecal butyrate levels were significantly higher in ASD children, though still within normal ranges. Network analyses illustrated that F. prausnitzii and Bacteroides species strongly co-occurred and correlated positively with ASD severity, measured through ADOS scores.

Key implications

The findings suggest that ASD in early childhood is associated with a restructuring of foundational gut microbial communities. Depletion of early colonizers such as B. longum alongside premature expansion of late colonizers like F. prausnitzii may reflect disrupted maturation of the gut ecosystem. These shifts influence metabolic output—notably butyrate production—and may interact with mucosal integrity, immune signaling, and neurodevelopment. Importantly, although butyrate levels were elevated, they remained physiologically normal, complicating simplistic assumptions about SCFA toxicity in ASD. Instead, the study underscores the need to examine microbial colonization timing, mucin degradation dynamics, and host–microbe metabolic cross-talk as mechanistic pathways relevant to ASD.

Citation

Coretti L, Paparo L, Riccio MP, et al. Gut microbiota features in young children with autism spectrum disorders.Front Microbiol. 2018;9:3146. doi:10.3389/fmicb.2018.03146