Manoogian, Juliana2024-05-152024-05-152024-05-15http://hdl.handle.net/10393/46220https://doi.org/10.20381/ruor-30348The prevalence of structural gastrointestinal diseases such as inflammatory bowel disease (IBD) and celiac disease (CE) are increasing in Canada. The gut microbiome is thought to be a factor involved in these diseases although its exact role remains unknown. We took two understudied avenues to further explore the role of the microbiome in these structural gastrointestinal diseases. First, we aimed to investigate the relationship between histone acetylation, specifically H3K27ac, and the gut microbiome in the context of pediatric IBD using an optimized protocol. The inhibition of histone deacetylase by butyrate is thought to be one pathway which may link butyrate-producing microbes with histone acetylation. We found H3K27ac binding to be increased in control patients near the enhancer regions of 2 genes which have previously been found to be involved in inflammation. We correlated H3K27ac and the microbiome and found negative correlations between genes and one microbe which was not necessarily a butyrate-producing microbe suggesting that the microbiome and epigenome axis may be more complex than simply through the inhibition of HDACs by butyrate. Second, we characterized the duodenal microbiome in the context of IBD and directly compared CD and CE, both avenues which have not been previously studied. We found that H2S-producing bacteria may be involved in CD at the duodenum and that gluten-degrading bacteria and related enzymes may be decreased in CE. Microbes associated with CD and CE were different from one another although further sequencing to achieve species differentiation would be required to confirm this. These studies characterized the microbiome and epigenome and allowed us to make predictions about how the microbiome may be involved in various functions within the context of IBD and CE.enCeliac DiseaseInflammatory Bowel DiseaseMicrobiomeEpigenomicsThesis