**4.5 Inflammatory bowel diseases**

Inflammatory bowel diseases (IBDs) refer to both ulcerative colitis (UC) and Crohn's disease, as well as other non-infectious inflammations of the bowel that are symptomatic of relapsing chronic disorders of the bowel [152]. There has been an increasing incidence of inflammatory bowel disease (IBD) globally. It has been commonly agreed that genetic susceptibility, external environment, microbial flora of the intestine, and immune responses are all components of IBD pathogenesis [153, 154]. Globally, IBD affects 4.2 million people, including 1.5 million Americans, and 2.2 million Europeans [154, 155]. First-degree relatives are five times more likely to develop IBD than those without IBD. There is a possibility that some genes are shared by both diseases since Crohn's Disease and UC can occur within the same family. In both diseases, environmental factor leads to triggering events [156]. In recent studies, 163 IBD-associated gene loci have been identified, of which 110 are associated with both diseases, 30 with Crohn and 23 with UC. Genetic analyses have revealed the essential role of autophagy in immune responses to IBD and identified two autophagy-related genes, ATG16L1 and IRGM [157–159]. Autophagy plays an important role in intracellular homeostasis, working to degrade cytosolic contents

## *Autoimmune Diseases of the GI Tract Part I: Etiology and Pathophysiology DOI: http://dx.doi.org/10.5772/intechopen.106184*

and organelles and resist infection, and eliminate microbes inside the cell. The coding mutation T300A is associated with an increased risk of Crohn since ATG16L1 is essential for all forms of autophagy [160]. Recent studies have demonstrated a link between IBD and IL23R (a coder for pro-inflammatory IL23 cytokine) [161]. IL23 is involved in Th17 cells [162]. IBD is well established to be caused by the Th17 and IL-23 pathway, with susceptibility loci for UC and Crohn, identified in IL23R, IL12B, JAK2, and STAT3 [163, 164]. The incidence and prevalence of IBD are increasing worldwide but are highest in westernized areas. In Europe, the highest prevalence values have been reported (ulcerative colitis 505 per 100,000 in Norway; Crohn's disease 322 per 100,000 in Germany). Several countries in Europe and North America have a prevalence of inflammatory bowel disease that exceeds 0.3%. Caucasians are prone to IBD more than Africans and Asians. Crohn is slightly more likely than UC to have a family history of the disorder, although both disorders are polygenic [165, 166]. The peak incidence for UC and Crohn is in the second to fourth decade, and no significance influence on prevalence by gender [167]. IBD patients compared to that in healthy control have unstable gut microbiota and it is often considered one of the triggering factors of IBD [168, 169]. There is a reduction in the diversity of microbiota in IBD, possibly making the host more vulnerable to pathogens or pathobionts colonizing it [170]. A high level of NO2 and SO2 correlate with an increased risk of IBD with elevated levels of air pollution. This is related to an increase in circulating polymorphonuclear leukocytes and plasma cytokines in IBD [171–173]. Environmental priming with triggering events is involved in manifestation of both diseases. Several triggers exist, including geography, social stress, a fast-paced lifestyle, smoking, diet, and drugs [174]. It has also been correlated that low vitamin is associated with IBD [175]. Stress has been commonly associated with IBD patients and it has been labeled as a trigger cause through multiple immunopathogenic pathways [176]. Persistent diarrhea with blood and mucous is a common symptom of IBD patients. The results of laboratory tests could be valuable in diagnosing IBD. Among the initial tests to be performed are complete blood count (CBC), renal function tests, liver enzyme tests, stools cultures, and C difficile toxin [156, 177].
