Pathophysiology
IBD is thought to result from a dysfunctional and chronic immune response to microbes in the gut, stemming from genetic susceptibility of the individual. While the exact causes of IBD remain largely unknown, it generally involves a complex interaction between 4 factors:
- Genetic
- Gut microbes
- Immune response
- Environment
Of the 4 components of IBD pathogenesis, the most rapid advances have been made in the genetic study of gut inflammation. Indeed, researchers have identified more than 200 genetic loci for IBD, which suggests that childhood- and adult-onset IBD overlap, with similar genetic predispositions.1-3
While genetics account for a portion of overall disease variance, microbial and environmental factors also interact with genetic elements in the pathogenesis of IBD. And with adaptive immune responses playing a major role in IBD pathogenesis, there are a variety of new and emerging targets of treatment.1-3
Current pathophysiological concepts of IBD not only help us better understand IBD but also illustrate the evolution of basic scientific concepts over time, with implications for developing new targeted therapies.4,5
References
- Zhang Y, Li Y. Inflammatory bowel disease: pathogenesis. World J Gastroenterol. 2014;20(1):91-99.
- Abraham B, Ahmed T, Ali T. Inflammatory bowel disease: pathophysiology and current therapeutic approaches. Handb Exp Pharmacol. 2017;239:115-146.
- Guan Q. A comprehensive review and update on the pathogenesis of inflammatory bowel disease. J Immunol Res. 2019;2019:7247238.
- Sartor R. Mechanisms of disease: pathogenesis of Crohn’s disease and ulcerative colitis. Nat Clin Pract Gastroenterol Hepatol. 2006;3(7):390-407.
- Rogler G, Biedermann L, Scharl M. New insights into the pathophysiology of inflammatory bowel disease: microbiota, epigenetics and common signalling pathways. Swiss Med Wkly. 2018; 148:w14599.
