The influence of fiber byproducts on bacterial invasion in pediatric inflammatory bowel diseases
The chronic, debilitating inflammatory bowel diseases (IBD), Crohn disease and ulcerative colitis, are diseases marked by inflammation and damage of the digestive tract with incidence rates rising rapidly in the pediatric population. IBD has a complex path of development and progression, with many contributing factors such as genetics, the environment, microbes, and the immune system. Though the exact cause is unknown, current evidence suggests that an environmental trigger leads to individuals with certain genes developing imbalances in their gut microbiome (the collection of microbes living in our digestive tract) and immune system with resulting disease. Diet has been shown to be the most influential environmental risk factor contributing to IBD, with fiber being an identified dietary component with significant impact on IBD risk and management. The gut microbiome plays an important role in the breakdown of fibers into their byproducts, short chain fatty acids (SCFAs). If individuals have an altered gut microbiome, as seen in IBD or prior to developing the disease, proper breakdown of fibers may be impaired, leading to changes in the gut environment such as with the composition of SCFAs. These environmental alterations caused by dietary patterns could stimulate normal bacteria to become invasive and contribute to IBD development. Since nutritional therapy is a first line treatment unique to pediatric IBD, further understanding of how diet interacts with the gut microbiome is critical to provide appropriate treatment for children with IBD. This study seeks to determine how SCFAs may influence bacterial invasion and contribute to IBD development and progression. Bacterial invasion will be assessed with a cell model utilizing patient-derived bacterial samples along with gut surface or immune cells. Results will help inform future dietary and therapeutic recommendations to treat IBD, especially in the pediatric population.