Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
+44 1223 790975
ISSN: 2155-9899
+44 1223 790975
Anita Annaházi and Tamás Molnár
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.