Genetics and pathogenesis of inflammatory bowel disease

This study looked at the genetics of inflammatory bowel disease (IBD) which arises from an excessive inflammatory response to microbes in the bowel. Healthy food metabolism depends on the co-evolution of the bacteria inhabiting our guts and our immune system; when these two fall out of since, our immune systems attack these helpful bacteria. Using GWAS, 99 different genetic risk loci (28 of which are similar to Crohn's disease) indicating the two arise from problems in the same pathway. The two forms of IBD, childhood-onset and adult-onset, seem to have similar genetic origins, implying other genetic, environmental, and epigenetic contributions to the disease. In addition, there is a weaker association between monozygotic twins having IBD than Crohn's disease (10-15% vs 30-35%). Some of the genes suspected to be involved in both Crohn's disease and IBD are those responsible for barrier function, microbial defense, innate immune regulation, regulation of adaptive immunity, ER stress and metabolism. The frequency of different variants of the disease varies in different populations indicating selective pressures of different environments. This study highlights the proteins involved in the digestive pathway, in addition showing promise for early disease diagnosis and treatment.