About the Topic
Inflammatory bowel diseases (IBD) include the two major forms Crohn’s disease (CD) and ulcerative colitis (UC). These disorders are characterized by episodes of inflammatory flares and periods of remission. IBD pose a substantial socio-economic burden to our healthcare systems: Patients typically suffer from abdominal pain, diarrhea, anemia, weight loss and fatigue, symptoms that may severely affect the quality of life and the ability to hold down an employment. IBD is a common inflammatory disease with more than 400.000 patients in Germany. IBD typically affects young people, with a peak disease onset between 15 and 30 years of age.
IBD currently cannot be cured
Since the cause of CD and UC are still unknown, there is currently no causative therapy available for patients with IBD. Clinical practice therefore aims at mitigating the symptoms associated with these diseases. Immunosuppressive drugs, such as corticosteroids that aim at downregulating the excessive immune responses within the intestinal mucosa, in general dominate IBD therapy. However, clinical practice demonstrates that currently available therapies induce remission only in subgroups of IBD patients. Moreover, many patients develop a steroid-resistant or steroid-dependent disease course upon long-term treatment with corticosteroids. Additionally, immunosuppressive agents such as azathioprine or cyclosporine A, which have been successfully used in IBD patients, are also effective in subgroups of patients only. In severe therapy-resistant cases, surgery is necessary to remove inflamed bowel parts in CD or the colon in UC.
A better understanding of the pathogenesis of IBD will lead to better treatment
IBD research aims at developing selective and specific drugs, which interfere with pathophysiologically important pathways, while at the same time leaving the patient as immunocompetent as possible. The downside of this approach is that development of targeted therapies requires a very detailed understanding of the pathophysiology of IBD in order to identify disease-specific mechanisms. Development of such targeted strategies is a major aim of TRR241.
Clinical practice demonstrates that individual patients respond to certain drugs while they do not respond to others. This observation indicates that there might be different causes of IBD and different pathomechanisms of mucosal inflammation may be present in patients. This concept implies that individual patients might benefit from different therapeutic regimes. In the future, clinical practice might therefore personalize drug therapies in order to provide each patient with the optimal drug.
“If you imagine the immune system as a big machine, we need to identify those gear wheels that connect the protective part of the immune system (that is necessary for defense against infections) from the part that drives chronic gut inflammation. These gear wheels might be excellent targets for future therapies.” – Christoph Becker