**1. Introduction**

Inflammatory bowel disease (IBD), including ulcerative colitis (UC), Crohn's disease (CD), and indeterminate colitis, is a chronic and relapsing inflammatory disorder of the gastrointestinal tract [1, 2]. More than 1 million residents in the United States and 2.5 million individuals living in Europe are estimated to be suffering from IBD [2]. The incidence of IBD has been rapidly increasing in newly industrialized countries in Asia, the Middle East, Africa, and South America over the last two decades [3, 4]. IBD has been associated with high morbidity and mortality, low quality of life, and financially demanding medical care [5]. The causes of this disease are multifactorial, the two main types: UC and CD, have similar clinical and

pathological presentations and can cause irreversible impairment of the structure and function of the gastrointestinal tract [6]. These diseases are characterized by a relapsing behavior, manifested by alternating phases of inactive states in which there is no intestinal inflammation and active states that present inflammation or any other disease symptoms [7]. Although the main biological processes involved in the development of both conditions are different [6]. CD can affect any part of the GI tract, especially the terminal ileum, associated with inflammation, stenosis, and/or fistulas [7, 8].

CD occurs in patients between the ages of 15 and 35 years, affects the mucosal layer of the colon, and causes abdominal pain, diarrhea, and fever, fistula, lesions in the rectum or intestine, and other symptoms. CD damages the small intestine; therefore, malnutrition is very common in CD [9]. Despite the UC, rectal bleeding is less common in CD patients and more than 50% of patients with CD suffer from folate and vitamin D deficiency, while more than 50% of people with UC suffer from iron deficiency [10].

UC disease is a mucosal inflammation that can only affect the large intestine, i.e., the colon, and the inflammation generally starts in the distal colon, going forward through the proximal colon until the cecum and can lead to ulcerations and bleeding [11]. About 25% of UC patients are diagnosed before the age of 18 years, because this disease affects adolescence [9]. There are different diagnostic tests for UC including clinical, endoscopic, histologic, and radiological tests although approximately 8.5% of IBDs are unclear [12, 13]. UC is the initial subtype of IBD, and the term IBD includes the characteristics of both CD and UC. It has long been difficult to distinguish between these two diseases, but now there is a clinical definition for both. Both diseases can affect specific parts of the lives of patients, such as school, job, social life, and family life **Figure 1** [9].

The concept of IBD pathogenesis is based on the theory of a disrupted intestinal barrier and a dysregulated immune response in a genetically susceptible host. IBD presents defects in the detection and control of the gut microbiota, associated with unbalanced immune reactions, genetic mutations that confer susceptibility to the disease, and complex environmental conditions such as a Westernized lifestyle [7, 14]. There is a strong clustering in families and with certain ethnicities. Other studies showed 15–50 times increased relative risk for siblings of a CD patient to also develop CD. The ethiopathology of IBD is multifactorial and is characterized by the interaction between genetic, microbial, environmental, and life style factors, which influences the immune responses and leads to the gut inflammation. Gut microbiota is important for the development and maturation of the immune system and reduced microbial diversity and its dysbiosis observed in IBD patients (**Figure 1**).

More than 200 IBD-associated susceptible genes have been identified, some of which are known to be involved or implicated in mediating host responses to gut microbiota [14]. This has evoked the possibility that gut microbiota is implicated in the pathogenesis of IBD [3]. Microbial factors have been historically proven to be indispensable for the onset of IBD, and advances in high-throughput sequencing have enabled us to elucidate the gut microbiome in IBD. IBD can be caused by determined infection of an enteric pathogen such as *Mycobacterium avium* subspecies paratuberculosis, *Clostridioides difficile, Helicobacter pylori*, *Campylobacter concisus*, *Fusobacterium nucleatum,* and adhesion-invasive *Escherichia coli*. An excess of translocation of intestinal bacteria across the intestinal barrier, the imbalance between beneficial and detrimental commensal bacteria can cause IBD [15, 16]. Some bacteria *Gut Microbiota and Inflammatory Bowel Disease DOI: http://dx.doi.org/10.5772/intechopen.105842*

**Figure 1.** *The effective agents in development of inflammatory bowel disease.*

including AIEC can be considered as both a persistent pathogen and detrimental commensal bacteria [17].

Therefore, this chapter covers the origins, causes, diagnosis, and treatment strategies of this complex disease.
