Emerging Role of Diet and Microbiota Interactions in Neuroinflammation

Abstract

Commensal gut microbiota exerts multifarious effects on intestinal and extra-intestinal immune homeostasis. A disruption in the microbial composition of the gut has been associated with many neurological disorders with inflammatory components. Here we review known associations between gut microbiota and neurological disorders. Further we highlight the emerging role of diet and microbiota interrelationship in regulating neuroinflammation.

Keywords: EAE; MS; diet; microbiome; neuroinflammation.

Figure 1

Diet-Microbiome interactions in neuroinflammation. Gut microbiota and dietary metabolites contribute to neuroinflammation through direct and indirect ways. Dietary fiber and tryptophan are modified by the microbiome to generate metabolites such as short chain fatty acids (SCFA) and indole derivatives which affects functional activity of local resident cells—the microglia and astrocytes. Tryptophan metabolites regulate the production of pro-and anti-inflammatory mediators like VEGF-B and TGF-α on microglia and Nos2, Ccl2, and Csf2 on astrocytes. SCFAs regulate the activation of microglia. In addition, bile acids, SCFAs, dietary salt and fatty acids directly induce differentiation of either T_H17 or T_reg cells. This may result in altered activity of inflammation associated molecules. T_H17 cells upregulate eNOS in CNS endothelia lining the blood vessels, thus altering blood brain barrier permeability. Bile acids may also penetrate the CNS and affect the activity of resident cells.