The discovery that commensal gut microbiota can influence host development and physiology beyond the gastrointestinal (GI) tract has triggered a paradigm shift in our conceptualization of the origin of human diseases. A growing body of preclinical research has demonstrated that gut microbiota exert a modulatory role on the development and function of brain circuits involved in motor control, emotion and cognition. These findings have lent support to the hypothesis that gut bacteria may play a role in the etiology and/or pathophysiology of human brain disorders. The current challenge is to understand the precise mechanisms mediating the communication between the microbiota and the brain. In the present thesis, we used a combination of mouse models (e.g., germ-free; GF, antibiotic treated, and transgenic mice), molecular, biochemical, and behavioral approaches to gain a deeper insight into the role of gut microbiota on brain development and behavior. A major goal was to explore whether microbial products from the commensal gut microbiota can be translocated into the developing brain and be sensed by pattern recognition receptors (PRRs) of the innate immune system.
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