Cong Hu, Heli Li, Yunjie Li, Shan Huang, Wenjia Wang, Feiyan Zhang, Yu Zhao, Yan Hao
Autism Spectrum Disorder (ASD) is characterized primarily by social deficits and repetitive behaviors, often accompanied by gastrointestinal dysfunction. Its etiology involves interactions among genetic, environmental, and biological factors. Current studies indicate that neuroinflammation and gut microbiota imbalance are key factors in the development of ASD. Neuroinflammation is characterized by elevated levels of pro-inflammatory factors and abnormal glial cell activation, whereas gut microbiota imbalance is evidenced by dysbiosis and compromised intestinal barrier function. The gut-brain axis regulates neuroinflammation and synaptic function through pathways such as short-chain fatty acids (SCFAs), tryptophan metabolism, γ-aminobutyric acid (GABA) metabolism, and the hypothalamic-pituitary-adrenal (HPA) axis. Although modulation of the microbiota, for example, fecal microbiota transplantation (FMT) and probiotics, could improve ASD symptoms by repairing the intestinal barrier and alleviating neuroinflammation, the molecular mechanisms underlying these effects remain to be elucidated. This article reviews the interaction between gut microbiota and neuroinflammation in ASD, aiming to provide insights for treatment and research.