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Research on autism spectrum disorders (ASDs) has so far focused primarily on the gut–brain axis, whereas the role of the gut–liver axis remains insufficiently explored. The aim of this study was to evaluate whether microbiota derived from girls with ASD induces dysbiotic changes in gut microbiota composition and leads to alterations in gut–liver axis processes in pseudo-germ-free (PGF) BALB/c mice. We also examined whether these processes could be modulated by altering the gut microbiota using the probiotic strains Lactiplantibacillus plantarum CCM 7512 and Limosilactobacillus reuteri CCM 8617 in combination with ground flaxseed (Linum usitatissimum L.) as a source of omega-3 polyunsaturated fatty acids and fermentable fiber. Colonization with fecal microbiota derived from girls with ASD resulted in dysbiotic changes in the composition of the cecal microbiota, characterized by an increased relative abundance of Escherichia–Shigella, Fusobacterium, Alistipes, and the Ruminococcus gnavus group. These changes were accompanied by impaired intestinal mucosal integrity, altered metabolomic pathways related mainly to aromatic amino acids and lipid metabolism, increased hepatic immunoreactivity of iNOS and COX-2, and elevated activity of the liver-specific LDH-5 isoenzyme. These results suggest that synbiotic intervention contributed to remodeling of the cecal microbiota composition, restoration of intestinal epithelial integrity, and modulation of metabolomic pathways, which was reflected by reduced immunoreactivity of iNOS and COX-2 in liver tissue and decreased activity of the LDH-5 isoenzyme. These findings support the role of microbiota-mediated metabolic processes in communication between the gut and the liver within the gut–liver axis.
Rodakova et al. (Tue,) studied this question.