The gut–brain axis, as a bidirectional communication network connecting the gut microbiota to the central nervous system, plays a key role in a variety of neurological and psychiatric disease processes. In recent years, researchers have discovered that bile acids (BAs) are important signaling molecules that extend beyond their traditional role in lipid digestion and absorption. They are now known to play a significant role in regulating metabolism, immunity, and nervous system functions. Notably, gut microbes dynamically regulate BA profile through deconjugation, dehydroxylation, and other biotransformations, building a complex regulatory network of microbial–host co-metabolism, which in turn modulates gut–brain axis function through multiple receptors. Specifically, BAs precisely regulate neuroimmune homeostasis, dynamic balance of the blood–brain barrier, and neurotransmitter metabolism through the activation of membrane and nuclear receptors, such as farnesoid X Receptor (FXR), takeda G protein-coupled receptor 5 (TGR5), pregnane X receptor (PXR), vitamin D receptor (VDR), and sphingosine-1-phosphate receptor 2 (S1PR2), a mechanism that provides a new perspective for elucidating the pathogenesis of neurological and psychiatric diseases. In this review, we systematically elucidate the microbial regulatory mechanisms of BA metabolism, focusing on the pathways through which BA–gut microbiota interactions affect neurological and psychiatric disorders via the neuroimmune pathway. By integrating the latest research evidence, we systematically sort out the key signaling pathways mediated by BA receptors and their neuroimmune regulatory networks, and provide a theoretical framework for the development of targeted intervention strategies for psychiatric disorders based on the regulation of the gut–brain axis.
Pei et al. (Sun,) studied this question.