The gastrointestinal (GI) tract harbors a highly diverse collection of microorganisms. The intestinal microbiota are involved in complex interactions between host mucosal epithelial and immune cells to shape fundamental physiological, metabolic, and immunological processes. Disruption to this symbiotic homeostasis and abnormal interactions between a host’s immune system and gut microbiota have been implicated in the pathogenesis of several chronic disorders, including inflammatory bowel disease (IBD), functional dyspepsia, irritable bowel syndrome, diabetes, obesity and autism.
In addition to behavioral symptoms of autism, reports of GI dysfunctions such as constipation, diarrhoea, and abdominal bloating are common. We note that not all autistic individuals suffer from gastrointestinal dysfunction; only a sub-population is affected. Although numerous intestinal microbial abnormalities have been identified in autism, conflicting results have often been reported. Overall, Firmicutes (70%), Bacteroidetes (20%) and Proteobacteria (4%) were most dominant phyla in the total sample. When autism group was divided according to gastrointestinal dysfunction, several significant microbial differences were apparent, although, these were not consistent across individuals and showed substantial variation. However, metabolites such as certain biogenic amines and sugars were found significantly elevated in autism group which suggest abnormal microbial metabolism in GI track.
Composition of the dominant microbiota in mouse model of IBD was disturbed, and prominent differences were evident at all levels of intestinal microbiome in fecal samples from Winnie mice, similar to observations inpatients with IBD. Metabolomic profiling revealed that chronic colitis in Winnie mice upregulated production of metabolites and altered several metabolic pathways, mostly affecting amino acid synthesis and breakdown of monosaccharides to SCFA. Significant dysbiosis in the Winnie mouse gut replicates many changes observed in patients with IBD. These results provide justification for the suitability of this model to investigate mechanisms underlying the role of intestinal microbiota and metabolome in the pathophysiology of IBD.The area of GI microbiota and functional metabolomics could be further explored for the potential treatment of chronic disease associate with GI dysfunctions.