The microbiota-gut-brain axis in gastrointestinal inflammation and neurological comorbidities

This article reviews the main literature published between April 2018 and March 2019 in the field of the microbiota-gut-brain axis focusing on gastrointestinal inflammation and neurological comorbidities. Over the last year, further evidence emerged relating to the existence of a bidirectional link between gastrointestinal inflammation in the form of inflammatory bowel diseases (IBD) and infection on the one hand, and neuroinflammation and neuropsychological changes on the other. Gastric Helicobacter infection, for instance, provoked neuroinflammation, characterized by activated microglia, which resulted in short-term memory loss. Furthermore, whereas anxiety and depression were associated with increased activity or development of IBD, a diseased activity at baseline was associated with an increased risk of evoking abnormally anxious behaviour. Colitis induction in animal models, by inducing dysbiosis and intestinal barrier disruption, confirmed the effect on the brain and vice versa with a central role for the brain-derived neurotrophic factor (BDNF). In addition, toll-like receptor (TLR) signaling has emerged as an important communication platform between the microbiota, the gut, and the brain. More specifically, the absence of TLR4 in mice partially protected the animals from the Parkinson’s disease-induced pathology. Furthermore, recent advances in the use of psychobiotics, referring to any exogenous influence whose effect on the brain is bacterially-mediated, highlighted an important role for Lactobacillus and Bifidobacterium spp., heat-inactivated microbial fermentates, and natural herbs to treat gastrointestinal and neurological disorders.