New evidences on the altered gut microbiota in autism spectrum disorders Original paper

What was studied?

This study investigated the altered gut microbiota in autism spectrum disorders (ASDs), a focus directly relevant to understanding microbiome signatures in clinical practice. Using amplicon-based sequencing of bacterial 16S rRNA (V3–V5) and fungal ITS1 regions, the researchers compared microbial community structures between autistic individuals and neurotypical controls. The goal was to define whether a distinct gut microbiome pattern—including both bacterial and fungal communities—characterizes ASDs and contributes to gastrointestinal symptoms frequently reported in this population. The study also assessed how constipation, a common ASD comorbidity, interacts with microbial composition.

Who was studied?

The research enrolled 40 autistic individuals, 90% of whom met criteria for severe ASD based on Childhood Autism Rating Scale scores, and 40 age- and sex-matched neurotypical controls. All participants consumed a Mediterranean-style diet and had not used antibiotics, probiotics, or prebiotics for at least three months prior to stool collection. Both groups included constipated and non-constipated individuals, enabling analysis of gastrointestinal symptoms independent of ASD diagnosis. Importantly, clinical markers of inflammation (calprotectin, ESR, serum IgA) showed no significant differences, suggesting microbiome shifts were not secondary to overt inflammatory disease.

Most important findings

Autistic individuals exhibited a markedly altered bacterial and fungal gut microbiota, forming a distinct community structure on beta-diversity analyses (as illustrated in the PCA plots on pp. 3–5). Bacterial findings included a significantly increased Firmicutes/Bacteroidetes ratio, driven by a reduction of Bacteroidetes (9.2% in ASD vs 19.4% in controls). Genera Alistipes, Bilophila, Dialister, Parabacteroides, and Veillonella were significantly depleted, while Collinsella, Corynebacterium, Dorea, and Lactobacillus were enriched in ASD. LEfSe cladograms (pp. 4–5) clearly depict these discriminant taxa. Constipated autistic individuals showed elevated Escherichia/Shigella and Clostridium cluster XVIII, taxa linked to inflammation and metabolite pathways that may exacerbate ASD-related GI symptoms. Neurotypical constipated individuals displayed different microbial associations, highlighting ASD-specific patterns.

Fungal analyses revealed an ASD-associated shift in gut mycobiota, with Candida species more than twice as abundant compared with controls (37.7% vs 14.1%), a trend visible in the fungal abundance plots. Although dispersion limited strict statistical significance, the clustering patterns showed Candida-enriched individuals were predominantly autistic. No meaningful bacterial-fungal correlations existed within ASD, suggesting a more decoupled dysbiosis.

Key implications

This study demonstrates that ASD is associated with a dual bacterial–fungal dysbiosis, independent of constipation and not explained by systemic inflammation. Reduced Bacteroidetes and enrichment of taxa previously linked to metabolic and inflammatory pathways suggest microbial contributions to ASD-related GI disturbances. Elevated Candida raises the possibility of fungal-driven immune modulation, including altered IL-22 and IL-17 responses, potentially sustaining dysbiosis. These findings underscore the need for microbiome-informed clinical strategies, including targeted modulation of both bacterial and fungal communities, and highlight the importance of microbiome-gut-brain interactions in ASD pathophysiology.

Citation

Strati F, Cavalieri D, Albanese D, et al. New evidences on the altered gut microbiota in autism spectrum disorders.Microbiome. 2017;5:24. doi:10.1186/s40168-017-0242-1