Between Dysbiosis, Maternal Immune Activation and Autism: Is There a Common Pathway?

Nutrients. 2024 Feb 16;16(4):549. doi: 10.3390/nu16040549.

Abstract

Autism spectrum disorder (ASD) is a neuropsychiatric condition characterized by impaired social interactions and repetitive stereotyped behaviors. Growing evidence highlights an important role of the gut-brain-microbiome axis in the pathogenesis of ASD. Research indicates an abnormal composition of the gut microbiome and the potential involvement of bacterial molecules in neuroinflammation and brain development disruptions. Concurrently, attention is directed towards the role of short-chain fatty acids (SCFAs) and impaired intestinal tightness. This comprehensive review emphasizes the potential impact of maternal gut microbiota changes on the development of autism in children, especially considering maternal immune activation (MIA). The following paper evaluates the impact of the birth route on the colonization of the child with bacteria in the first weeks of life. Furthermore, it explores the role of pro-inflammatory cytokines, such as IL-6 and IL-17a and mother's obesity as potentially environmental factors of ASD. The purpose of this review is to advance our understanding of ASD pathogenesis, while also searching for the positive implications of the latest therapies, such as probiotics, prebiotics or fecal microbiota transplantation, targeting the gut microbiota and reducing inflammation. This review aims to provide valuable insights that could instruct future studies and treatments for individuals affected by ASD.

Keywords: autism spectrum disorders; brain–gut axis; delivery; dysbiosis; gastrointestinal; gut microbiota; maternal immune activation (MIA); microglia; neurodevelopment; short-chain fatty acids (SCFA).

Publication types

  • Review

MeSH terms

  • Autism Spectrum Disorder* / etiology
  • Autism Spectrum Disorder* / metabolism
  • Autistic Disorder* / etiology
  • Bacteria
  • Child
  • Dysbiosis / complications
  • Family
  • Gastrointestinal Microbiome* / physiology
  • Humans

Grants and funding

This study was supported by the Medical University of Bialystok, grant number B.SUB.24.445. The financial sponsor played no role in the design, execution, analysis, and interpretation of data.