The ecosystem of microorganisms that inhabit the human gastrointestinal tract, termed the gut microbiota, critically maintains host homeostasis. Alterations in species structure and metabolic behaviour of the gut microbiota are thus unsurprisingly exhibited in patients of gastrointestinal disorders when compared to the healthy population. Therefore, strategies that aim to remediate such gut microbiota through microbial supplementation have been attempted, with variable clinical success. Clearly, more knowledge of how to assemble a health promoting gut microbiota is required, which could be drawn upon from the framework of ecological theory. Current theories suggest that the forces driving microbial community assembly include historical contingency, dispersal limitation, stochasticity and environmental selection. Environmental selection additionally encompasses habitat filtering, i.e., host-microbe interactions, and species assortment, i.e., microbe-microbe interactions. I propose to explore the application of this theory to the human gut microbiota, and I hypothesize that microbial ecological theory can be replicated utilizing complex defined microbial communities. To address my hypothesis, I first built upon existing methods to assess microbial community composition and behaviour, then applied such tools to human fecal-derived defined microbial communities cultured in bioreactors, for example, by using marker gene sequencing and metabonomics. I determined that stochasticity is an important influencer of species structure within the gut microbiota, whereas dietary interventions greatly impacted the metabolic behaviour. Additionally, habitat filtering predominated over species assortment. This assertion was based on the lack of competitive exclusion observed when beneficial microbes were added to an ulcerative colitis-associated microbial community with and without prior antibiotic treatment. The few unique functionalities that were provided by these microbes upon integration are related to starch and mucin degradation. Also, there was not a discernible overall difference between a microbial community and its non-coevolved species matched counterpart, in which each species was derived from a separate donor. However, the existence of species assortment was not precluded, since certain species that relied upon cross-feeding for polysaccharide utilization failed to integrate into the non-coevolved microbial community. Together, this work would suggest that successful modulation of the gut microbiota would involve providing microbes as coevolved guilds that can colonize niches ubiquitous amongst the human population.