Inflammatory bowel diseases (IBD) are a collection of diseases characterized by chronic gastrointestinal inflammation resulting from an exuberant immune response to commensal flora in genetically susceptible individuals. Rapid advances in the field of genomics have resulted in the identification of at least 163 loci that contribute susceptibility to both Crohn’s disease (CD) and ulcerative colitis (UC). Similar to other complex diseases, however, the “curse of missing heritability” remains a significant concern in understanding the mechanisms underlying IBD. While genetic discoveries, to date, only account for 7–14 % of disease variance for IBD, studies have increasingly demonstrated a role for environmental factors in disease pathogenesis. Furthermore, the use of animal models of IBD has led to a greater understanding of disease pathogenesis implicating various aspects of the innate immune response including the bacterial, fungal, and viral microbiome and adaptive immune response such as the interleukin (IL)-23/IL-17 pathway.

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