Neuroinflammation in the Brain and Role of Intestinal Microbiota: An Overview of the Players

Great interest is aimed at understanding the inflammatory responses at the level of the central nervous system (CNS), referred to as neuroinflammatory. The environment and the duration of the inflammatory responses are essential factors for comprehending the biochemical and pathophysiological consequences induced by the inflammatory state. Specific inducers of inflammation associated with neurodegenerative disorders can activate inflammatory processes and produce mediators that potentiate neurodegeneration. Immune responders in the brain include microglial cells, astrocytes, and mast cells. A number of human pathologies are recognized to have an inflammatory component, including disorders related to brain function. Emerging evidence also attributes an important role to intestinal microorganisms in disorders related to brain function. In the gut-brain axis, the intestinal microbiota produce a variety of molecules and neurotransmitters, transform primary bile acids into secondary bile, and synthesize short-chain fatty acids. Communication within the gut-brain axis occurs through several pathways, including the immune system, the enteric nervous system, the vagus nerve, and the production of microbial metabolites. The CNS responds to this input from the gut by modulating the activity of the autonomic nervous system and the hypothalamic-pituitary-adrenal axis, which manages adrenocortical hormones. In this perspective, gut microbiota may influence neural function by influencing microglia, astroglia, and mast cells. Conversely, the relationship between neurons, microglia and synaptic alteration may also involve gut microbiota. The purpose of this review is to provide a concise overview of the mechanisms involved in communication between intestinal microbiota and the brain and how this contributes to the management of neuroinflammation.