## 2 Inflammatory Bowel Disease  
Inflammatory bowel disease (IBD) is a chronic idiopathic disease of the GI tract, which encompasses several diagnoses such as Ulcerative colitis (UC), Crohn's disease (CD), and Indeterminate colitis (IC) [1]. IBD typically manifests as ulcerations in varying regions of the GI tract; UC is primarily found to affect the mucosal layers of the colon in a continuous pattern, while CD may affect any part of the gastrointestinal (GI) tract in non-continuous form and IC patients are those in which neither a diagnosis of UC or CD can be determined but still present with characteristics of IBD [2]. Cardinal symptoms of IBD include diarrhea, rectal bleeding, fatigue, abdominal pain, unintended weight loss, decreased appetite, and vomiting [3]. However, disease presentations can vary extensively from patient-to-patient and overlaps with other GI conditions, such as irritable bowel syndrome [1]. The pathogenesis of IBD remains fundamentally indeterminate; however, it is believed to be a delicate interplay between a multitude of factors including GI immune dysregulation, genetic predisposition, gut microbiota dysbiosis, and environmental factors [4; 5]. For example, in a large-sample based genome-wide association study (GWAS) published in 2016, several gene variant associations were found in the chronic immune-mediated diseases CD, UC, psoriasis, and primary sclerosing cholangitis [6]. This study presented evidence for overlap of genetic susceptibility loci of these diseases, which may be contributed to biological pleiotropy [6]. Thus, pleiotropy and gene variants could be a factor in understanding IBD pathogenesis and identifying genetically susceptible individuals. Although genetic susceptibility has been shown to contribute to IBD pathogenesis, environmental risk factors at play seem to be a major contributor to the majority of diagnosed IBD patients [7]. Environmental risk factors have the ability to impact gut microbiota in IBD pathogenesis as well, and include antibiotics and other medication use, tobacco use, diet, socioeconomic status [8], and psychological stressors [8] however it is difficult to determine whether microbiota shifts are the cause or consequence of these environmental factors. IBD affects multiple ethnic and racial groups, with onset of disease occurring throughout early adulthood between the ages of 20-40 [9; 10; 11] with approximately 0.4-0.6% of cases being reported globally [12; 13]. While data is still lacking for many developing countries, increases in IBD prevalence appears to be paralleled with increasing development index [13] as the incidence of UC is highest in North America with 16.4 new cases per 100,000 people annually and 16.7 per 1000 people in Canada [8]. The Western diet is considered a major contributor to the obesity epidemic and is concurrently a major risk factor in IBD pathogenesis [14]. Therefore, not surprisingly, the incidence of IBD is highest in Westerized countries [8]. Additionally, diet has been associated with which gut microbes will thrive and those that will not [15]. Microbial dysbiosis has been implicated as a major pathophysiological mechanism in IBD contributing to a perpetuating feedback loop of dysregulated host-microbiota shifts [16]. As the incidence of IBD continues to rise globally, and across new populations, such as in children [1], the need for effective treatment options, diagnostics, and understanding of the pathophysiology mechanisms become more prudent. Treatments for IBD include several classes of drug therapy, i.e., immunosuppressants, corticosteroids, aminosalicylates, and, more recently, monoclonal antibodies, in addition to palliative treatments like antibiotics, analgesics, anticholinergics, and antidiarrheal agents [3; 9; 17].