Abstract

The gut microbiome is a community of closely interacting microbes living in the gastrointestinal tract. Its structure has direct relevance to health. Disturbances to the microbiome, such as due to antibiotic use, have been implicated in various diseases. The goal of this study was to determine how the gut microbiome reacts to and recovers from disturbance caused by antibiotics. Because diet also influences the microbiome, this study included the interaction between diet and antibiotics. Half of the mice in each diet treatment were given antibiotics to disturb their microbiomes. After cessation of antibiotics, mice were paired in combinations within diets to determine whether the microbiomes of control mice influenced the disturbed microbiomes of formerly antibiotic mice. Chapter 1. Diet significantly altered the structure of the gut microbiome but its effect was significantly smaller than the effect of antibiotics. There was a significant interaction between diet and antibiotics; the antibiotic effect was larger in the cornstarch diet than in the glucose diet. Dysbiotic microbiomes resulting from antibiotics were characterized by an increase in Bacteroidetes and Proteobacteria, and a decrease in Firmicutes. Antibiotic administration also resulted in an initial increase OTU diversity, mainly because it reduced the abundance of dominant OTUs, resulting in greater evenness. Chapter 2. Seven weeks after the cessation of antibiotics (experiment termination), the effect of the antibiotics on the microbiome was still evident. The structure of the dysbiotic microbiome had not returned to that of control mice. Antibiotics significantly increased the relative abundance of some taxa and significant decreased the relative abundance of others. It was unexpected that the taxonomic hierarchy within the microbiome did not recover after 7 weeks following cessation of antibiotics. It would appear, therefore, that antibiotics established a new, semi-stable hierarchy. Chapter 3. When paired together, the assumption was that dysbiotic microbiomes of antibiotic mice would be positively influenced by microbiomes of control mice, based on the assumption that the control mouse would act as a probiotic for the antibiotic mouse, either via coprophagy or consumption of food contaminated by feces. Contrary to that hypothesis, the microbiomes of control mice became more similar to that of antibiotic mice. One can offer at least two hypotheses to explain this result, but neither was tested. First, compared to the control microbiome, the dysbiotic microbiome may have been more stable and thus more resistant to change due to invasion by OTUs from the control microbiome. Other research has shown that dysbiotic microbiomes have a high degree of stability. If this were true, the use of probiotics is questionable. Second, one or more of the antibiotics could still have been active at the initial phase of pairing, and coprophagy caused the microbiome of the control mice to rapidly become dysbiotic. If this is true, the experiment should have been conducted with a waiting period between the cessation of antibiotic administration and pairing.

Degree

College and Department

Life Sciences; Biology

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