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Ulcerative Colitis and Crohn’s disease are increasingly common inflammatory bowel diseases (IBD). Scientists of the University Medical Center Hamburg-Eppendorf (UKE), Yale University and the Collaborative Research Centre 841 (CRC 841) have identified a novel molecular mechanism that contributes to intestinal tissue damage and inflammation. In addition, these results pave the way for the development of more specific immunotherapy. The findings of the study are to be published in Science tomorrow.
The primary cause that initiates IBD is still unclear. However, it is well-accepted that inflammatory responses, most likely driven by the intestinal microbiome and a defective barrier function, promote a vicious cycle that leads to development of chronic disease. Since IBD is characterized by chronic inflammation, most of its therapies nowadays are being directed against these inflammatory responses, but cannot or do not directly promote mucosal healing. Relapsing flares and opportunistic infections that often occur as a consequence of the immune suppression are the resulting problems. Thus one major goal in the field of chronic inflammation, especially in IBD, is to identify the exact mechanisms that link inflammation and barrier dysfunction. Scientists from Hamburg and Yale have now made a significant progress in this regard. Prof. Dr. Samuel Huber, I. Department of Medicine, University Medical Center Hamburg-Eppendorf, and one of the leading scientists of the study, explains: "We were able to show that a dysregulation of the IL-22-IL-22BP-axis is involved in the development of IBD. The function of Interleukin 22 (IL-22) is to promote healing of damaged intestinal mucosa. However, interleukin 22 binding protein (IL-22BP), the soluble antagonist of IL-22, is over expressed by CD4+ T cells in the intestine of IBD patients. Thus IL-22 cannot exert its tissue protective function."
These data could pave the way for future therapies. "Our data imply that targeting IL-22BP directly might allow for a more effective and specific therapy of IBD without invoking the undesirable and potentially dangerous side effects of current immune suppressive therapies such as susceptibility to infections." says Huber.
Furthermore, it is suggested that a dysregulation of the IL-22-IL-22BP-axis does not only play an important role in IBD but also in other chronic diseases. "The question why diseases become chronic is an important research issue of the CRC 841. These new findings will make a decisive impact on research into inflammation and autoimmune diseases," says Prof. Dr. Ansgar W. Lohse, Director of the I. Department of Medicine, University Medical Center Hamburg-Eppendorf, and spokesperson of the CRC 841, which partially funds the interleukin research.
The success of the research is owed to a close scientific cooperation: In addition to the group of Prof. Dr. Samuel Huber, the group of Prof. Dr. Nicola Gagliani at the I. Department of Medicine as well as the Medical Clinic and Polyclinic for General, Visceral and Thoracic Surgery, both at University Medical Center Hamburg-Eppendorf, and Prof. Dr. Richard A. Flavell at the Yale University, USA, participated in leading roles in this study.
A video interview with Prof. Huber on current IL-22/IL-22BP research: http://www.sfb841.de/english/homepage.html
Literature:
Penelope Pelczar, Mario Wittkowski, Laura Garcia Perez et al., A pathogenic role for T-cell derived IL-22BP in inflammatory bowel disease.
http://science.sciencemag.org/cgi/doi/10.1126/science.aah5903
Contact:
Prof. Dr. Samuel Huber
I. Medizinische Klinik und Poliklinik
Universitätsklinikum Hamburg-Eppendorf (UKE)
Martinistraße 52
20246 Hamburg
Telephone: (040) 7410-57273
E-mail: s.huber@uke.de
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