Abstract
Dysbiosis secondary to environmental factors, including dietary patterns, antibiotics use, pollution exposure, and other lifestyle factors, has been associated to many non-infective chronic inflammatory diseases. Autism spectrum disorder (ASD) is related to maternal inflammation, although there is no conclusive evidence that affected individuals suffer from systemic low-grade inflammation as in many psychological and psychiatric diseases. However, neuro-inflammation and neuro–immune abnormalities are observed within ASD-affected individuals. Rebalancing human gut microbiota to treat disease has been widely investigated with inconclusive and contradictory findings. These observations strongly suggest that the forms of dysbiosis encountered in ASD-affected individuals could also originate from autonomic nervous system (ANS) functioning abnormalities, a common neuro–anatomical alteration underlying ASD. According to this hypothesis, overactivation of the sympathetic branch of the ANS, due to the fact of an ASD-specific parasympathetic activity deficit, induces deregulation of the gut–brain axis, attenuating intestinal immune and osmotic homeostasis. This sets-up a dysbiotic state, that gives rise to immune and osmotic dysregulation, maintaining dysbiosis in a vicious cycle. Here, we explore the mechanisms whereby ANS imbalances could lead to alterations in intestinal microbiome–host interactions that may contribute to the severity of ASD by maintaining the brain–gut axis pathways in a dysregulated state.
Highlights
The clinical manifestation of autism spectrum disorder (ASD) is frequently associated with gastrointestinal (GI) dysbiosis that is unrelated to dietary habits and is often manifested by altered bowel habits and chronic abdominal pain [1,2]
The consequence would be a decrease in the secretion of bactericidal peptides and metabolites from Paneth cells, goblet cells, and intestinal mucosal surface phagocytes, such as macrophages, which coexist with microbial communities [61]
This would lead to the loss of commensal microbial populations and the simultaneous deregulation of luminal ionic and water homeostasis, resulting in the highly heterogeneous and polymorphic dysbioses with unusually high incidences observed in ASD [26]
Summary
The clinical manifestation of autism spectrum disorder (ASD) is frequently associated with gastrointestinal (GI) dysbiosis that is unrelated to dietary habits and is often manifested by altered bowel habits and chronic abdominal pain [1,2]. The only consistent observations appear to be a significant decrease in overall bacterial diversity together with an increased presence of the Bacteroidetes phylum (Gram-negative, nonspore-forming, and anaerobic), leading to the imbalance of the Bacteroidetes/Firmicutes (Gram-positive, spore-forming, and obligate or facultative aerobes bacilli) ratio (B/F ratio). This very same observation (increased B/F ratio) has been reported in studies addressing depressive patients [5,6] as well as in depressive-like rat models [7,8]. The genera most frequently reported as overrepresented include the Clostridium genus [9,10,11,12,13,14,15,16]
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