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Understanding the Multidirectional Axes of Communication Between the Gut Microbiome and the Brain to Augment Human Performance

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Technical Report,10 Dec 2016,09 Dec 2019

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The overall goal of this project was to characterize host-microbe interactions following an acute stressor and examine whether this interactionmediates host stress recovery via mechanisms of the microbiota-gut-brain axis. Our hypothesis was based on the principle that acute stress will modulate host-microbe interactions at the level of the gastrointestinal tract as the host responds to and recovers from that stressor and that identifiable patterns of host-microbe crosstalk would yield a molecular signature predictive of, and useful in modulating, host behavioural and cognitive outcomes via the microbiome-gut-brain axis. We have characterized aspects of recovery from acute stress using common stress-related readouts in male and female conventionally-raised, germ-free GF, as well as ex-GF i.e. GF mice that have been colonized with a conventionally-raised murine microbiota mice. Substantial differences in the reaction and recovery of the enteric L-tryptophan metabolic pathway were identified in the gastrointestinal tracts of conventional and GF mice of both sexes. Specifically, the conversion of L-tryptophan to neuroactive molecules, including the neurotransmitter serotonin, was significantly elevated post-stressor in the colon of the gastrointestinal tract of male but not female conventional mice. This stress-induced effect was absent in GF male mice but was restored in ex-GF mice, thereby highlighting a role for the microbiome in influencing stress-responsivity at the level of the gastrointestinal tract. Metabolomic profiling revealed that levels of tryptophan in the cecum decreased after stress in all groups.

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  • Stress Physiology
  • Biochemistry

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