A new study is helping researchers understand why the microbiome – the collection of trillions of organisms living together in the gut – changes during a bout of Irritable Bowel Disorder and how this results in an unnecessary inflammatory reaction.
Researchers from Harvard T.H. Chan School of Public Health and the Broad Institute of MIT and Harvard followed 132 participants over the course of year. Blood and stool samples and colon biopsies from participants with Crohn’s disease and ulcerative colitis were compared to a group of people who did not have IBD. More than 2,965 samples were collected, providing unparalleled molecular, cellular, and clinical tools to help researchers understand the detailed biochemistry of the disease.
Data revealed that during periods of disease activity, people with IBD had fewer microbially-derived chemicals. Researchers believe this could be due to a combination of factors, including poorer nutrient absorption, greater water content or blood flow in the bowels, less beneficial microbial metabolism, and more urgent bowel movements. Overall, these factors made the microbiome less stable and led to more improper immune responses and flare-ups among IBD patients.
More specifically, stool samples from individuals with IBD showed high levels of polyunsaturated fatty acids, the presence of nicotinic acid (which was not present in samples from individuals who did not have IDB), and depleted levels of vitamins B5 and B3.
Overall, the results from this study provides the most in-depth data on the microbiome of individuals with IBD. The findings will be used to propel future research and discover new treatments for those living with the disease.
"Given how tightly connected the microbiome is with our health and wellbeing, these results shed some light on how we might avoid the problems that arise when this relationship goes awry, and how we might be better stewards of these life-long companions," said Jason Lloyd-Price, a research scientist at Harvard Chan School and the Broad Institute and lead author of the paper.