Pathogenesis of Ulcerative Colitis and Crohn’s Disease: Similarities, Differences and a Lot of Things We Do Not Know Yet

Abstract

The pathogenesis of inflammatory bowel diseases (IBD), such as ulcerative colitis (UC) and Crohn's disease (CD) is complex, and our knowledge on the topic is constantly growing. The two disorders are distinct, yet overlap in their clinical manifestations and underlying causes. This review aims to provide a broad overview of the numerous pathogenetic factors that can lead to the development of IBD, focusing on novel findings and on the differences between UC and CD. Recent advances in genetics have identified new components in the pathogenesis, as an example, the importance of Th17 lymphocytes and the IL-17/IL-23 pathway have been highlighted in both diseases, apart from the previously known Th1-Th2 driven processes. Genetic background of increased permeability has been explored in UC, and the role of defective autophagy was recently described in CD. Genetic alterations can lead to an exaggerated immune response to the resident microbial flora. This microflora is altered in IBD patients, probably due to their reduced ability to stabilize its bacterial components and due to different environmental factors. An exhaustive exploration of environmental factors is particularly important, as they can be influential in many cases. The impact of smoking is the most established environmental factor, having deleterious effects in CD and protective in UC. Recent opinions on other factors, such as early appendectomy, diet, reduced vitamin D levels, the use of specific medications, breastfeeding, personal hygiene and psychological factors are also discussed. Epigenetics, a new field of research, links environmental factors to genetics. Understanding these factors is of great significance as changing lifestyles and improving life circumstances have started to increase the prevalence of IBD also in developing countries.

MiRNAs and inflammatory bowel disease: An interesting new story

“…The interactions of the host and the bowel germs can be beneficial or harmful to both parties and cause inflammation of the intestine. Observations in patients with IBD and animal models indicate the role of bacteria in inflammation; in other words, the presence of bowel bacteria is necessary for inflammation (Annaházi & Molnár, 2014;Kaser et al, 2009;Podolsky, 1991).…”

“…The interactions of the host and the bowel germs can be beneficial or harmful to both parties and cause inflammation of the intestine. Observations in patients with IBD and animal models indicate the role of bacteria in inflammation; in other words, the presence of bowel bacteria is necessary for inflammation (Annaházi & Molnár, ; Kaser et al, ; Podolsky, ). Intestine epithelium is a barrier between intestinal germs and the lymphoid tissue associated with the gastrointestinal system, which plays an essential role in the formation of mucosal immune response (Podolsky, ).…”

Expression Profile of p53 and p21 in Large Bowel Mucosa as Biomarkers of Inflammatory-Related Carcinogenesis in Ulcerative Colitis

“…Over time, epithelial colonic cells suffer from genomic instability induced by oxidative stress, linked to chronic inflammation. Inflammatory infiltrate in UC generates oxygen radicals and nitrogen species that affect numerous metabolic processes involved in cell repair [11, 12]. …”

Plants with Anti-Ulcer Activity and Mechanism: A Review of Preclinical and Clinical Studies

“…It also aims to promptly initiate and sustain a state of remission over an extended period. 55 , 56 The primary negative consequences encompass gastrointestinal disruptions such as feelings of nausea, vomiting, constipation, and diarrhea, as well as impacts on the cardiovascular system. 10 …”

“…It also aims to promptly initiate and sustain a state of remission over an extended period. 55,56 The primary Bethanechol Vehicle (Distilled water 3%) as a negative control and 5-aminosalicylic acid (ASA) (400 mg/ kg) as a positive control.…”