The Inflammatory Bowel Diseases Research Group - CEMIR
Inflammatory Bowel Diseases (IBD)
The Inflammatory Bowel Diseases Research Group aims at understanding central mechanisms for mucosal homeostasis and how this is disrupted in active disease and subsequently restored in remission.
The inflammatory bowel diseases (IBD) research group studies disease mechanisms in IBD, and use this knowledge to improve diagnostics and prognostics. Another central aim is to discover novel therapeutic targets. More specifically, the IBD projects concentrate on understanding central mechanisms for mucosal homeostasis and how these are disrupted in active disease and subsequently restored in remission.
Example projects are the effect of hypoxia on the epithelium, the role of guanylin/uroguanylin in inflammation, the action and regulation of mucosal antimicrobial peptides and how the diffuse neuroendocrine system interacts with immune signaling in inflammatory bowel diseases.
Research documentation
- Chin A, Svejda B, Gustafsson BI, Granlund A vB, Sandvik AK, Timberlake A, Sumpio B, Pfragner R, Modlin IM, Kidd M. The role of mechanical forces and adenosine in the regulation of intestinal enterochromaffin cell serotonin secretion. Am J Physiol 2012, 302, G397-G405
- Østvik AE, Granlund AvB, Bugge B, Nilsen NJ, Torp SH, Waldum HL, Damås JK, Espevik T, Sandvik AK. Enhanced expression of CXCL10 in inflammatory bowel disease – potential role of mucosal Toll-like 3 receptor stimulation. Inflammatory Bowel Diseases, 2013, 19(2), 265-274
- Granlund AvB, Flatberg A, Østvik AE, Drozdov I, Gustafsson B, Kidd M, Beisvåg V, Torp SH, Waldum HL, Martinsen TC, Damås JK, Espevik T, Sandvik AK. Whole Genome Gene Expression Meta-analysis of Inflammatory Bowel Disease Colon Mucosa demonstrates lack of major differences between Crohn's Disease and Ulcerative Colitis. PLoS ONE 2013 8(9): e76234. doi:10.1371/journal.pone.0076234
- Østvik AE, Granlund AvB, Torp SH, Flatberg A, Beisvåg V, Waldum HL, Flo TH, Espevik T, Damås JK, Sandvik AK. Expression of Toll-like receptor 3 is enhanced in inflammatory bowel disease and mediates the excessive release of lipocalin 2. J Clin Exp Immunol 2013, 173(3), 502-511
- Østvik AE, Granlund AvB, Gustafsson BI, Torp SH, Espevik T, Mollnes TE, Damås JK, Sandvik AK. Mucosal Toll-like receptor 3-dependent synthesis of complement factor B and systemic complement activation in inflammatory bowel disease. Inflammatory Bowel Diseases 2014, 20(6), 995-1003
- Silje Thorsvik Atle van Beelen Granlund Tarjei D Svendsen Ingunn Bakke Elin S Røyset Trude H Flo Jan K Damås Ann E Østvik Torunn Bruland Arne K Sandvik. Ulcer‐associated cell lineage expresses genes involved in regeneration and is hallmarked by high neutrophil gelatinase‐associated lipocalin (NGAL) levels. First published: 11 February 2019 https://doi.org/10.1002/path.5258
- Skovdahl HK, Granlund AvB, Østvik AE, Bruland T, Bakke I, Torp SH, Damås JK, Sandvik AK. CCL20 and its corresponding receptor CCR6 expression is enhanced in active inflammatory bowel disease and TLR3 mediates CCL20 expression in colonic epithelial cells. PloS One 2015, Nov 4;10(11):e0141710. doi:10.1371/journal.pone.0141710
- Brenna Ø; Furnes MW; Munkvold B, Kidd M; Sandvik AK; Gustafsson BI. Cellular localization of guanylin and uroguanylin mRNA in human and rat duodenal and colonic mucosa. Cell Tissue Res 2016, 365, 331-341.
- Thorsvik T, Damås JK, Granlund AvB, Flo TH,, Østvik AE, Sandvik AK. Fecal Neutrophil Gelatinase Associated Lipocalin (NGAL) as a biomarker for Inflammatory Bowel Disease. J Gastroenterol Hepatol 2017, 32, 128-135.
- Catalan-Serra I, Sandvik AK, Bruland T, Andreu-Ballester JC. Gammadelta T cells i Crohn’s disease: A new player in the disease pathogenesis? Journal of Crohn’s and Colitis, in press
Group Leader
Collaboration
- Noah Wolcott Palm, Ass. professor, Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA
- David Underhill, Professor, Cedars-Sinai Medical Center, Los Angeles, CA, USA
- Anis Larbi, Ph.D. Principal Investigator, Biology of Aging Program, Biomedical Sciences Institutes: Agency for Science, Technology and Research (A*STAR), Singapore
- Jon Florholmen, Professor, Gastroenterology and Nutriton Research Group, Department of Clinical Medicine, University of Tromsø, Norway