S Vatn1,2, A Carstens3,4, A B Kristoffersen5, D Bergemalm3, C Casén5, A E F Moen2,6, T M Tannaes2,6, J Lindstrøm2,7,8, T E Detlie1,2, C Olbjørn2,9, C M Lindquist3, J D Söderholm10, F Gomollón11, R Kalla12, J Satsangi12, M H Vatn2, J Jahnsen1,2, J Halfvarson3, P Ricanek1. 1. Department of Gastroenterology, Division of Medicine, Akershus University Hospital, Lørenskog, Norway. 2. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. 3. Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden. 4. Department of Internal Medicine, Ersta Hospital, Stockholm, Sweden. 5. Genetic Analysis AS, Oslo, Norway. 6. Department of Clinical Molecular Biology (EpiGen), Division of Medicine, Akershus University Hospital, Lørenskog, Norway. 7. Health Services Research Unit, Akershus University Hospital, Lørenskog, Norway. 8. Department of Pediatric and Adolescent Medicine, Akershus University Hospital, Lørenskog, Norway. 9. Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. 10. Digestive Diseases Unit, IIS Aragón, Zaragoza, Spain. 11. Gastrointestinal Unit, Centre for Genomics and Molecular Medicine, Division of Medical and Radiological Sciences, University of Edinburgh, Edinburgh, UK. 12. Translational Gastroenterology Unit, Medical Sciences/Experimental Medicine Division, University of Oxford, Oxford, UK.
Abstract
METHOD: We examined faecal samples, using the GA-map™ Dysbiosis Test, to associate gut microbiota composition with Crohn's disease (CD) and ulcerative colitis (UC) and to identify markers for future biomarker identification. We conducted a prospective case-control study (EU-ref. no. 305676) in an inception cohort of 324 individuals (64 CD, 84 UC, 116 symptomatic non-IBD controls and 44 healthy controls) across five European centres and examined 54 predetermined bacterial markers. We categorized patients according to the Montreal Classification and calculated the dysbiosis index (DI). Non-parametric tests were used to compare groups and the Bonferroni correction to adjust for multiple comparisons. RESULTS: The fluorescent signals (FSSs) for Firmicutes and Eubacterium hallii were lower in inflammatory bowel disease (IBD) vs. symptomatic controls (p<.05). FSS for Firmicutes, Lachnospiraceae, Eubacterium hallii and Ruminococcus albus/bromii were lower, whereas the signal for Bacteroides Fragilis was higher in UC vs. symptomatic controls (p<.05). FSS was higher for Bifidobacterium spp., Eubacterium hallii, Actinobacteria and Firmicutes among patients with ulcerative proctitis, compared to extensive colitis (p<.05). In CD, we observed no association with disease location. The DI correlated with faecal-calprotectin in both CD and in UC (p<.001). In terms of treatment escalation and anti-TNF response, differences were observed for some bacterial markers, but none of these associations were statistically significant. CONCLUSION: Our data reveal that the GA-map™ Dysbiosis Test holds the potential to characterize the faecal microbiota composition and to assess the degree of dysbiosis in new-onset IBD. On the other hand, our results cannot demonstrate any proven diagnostic or predictive value of this method to support clinical decision making.
METHOD: We examined faecal samples, using the GA-map™ Dysbiosis Test, to associate gut microbiota composition with Crohn's disease (CD) and ulcerative colitis (UC) and to identify markers for future biomarker identification. We conducted a prospective case-control study (EU-ref. no. 305676) in an inception cohort of 324 individuals (64 CD, 84 UC, 116 symptomatic non-IBD controls and 44 healthy controls) across five European centres and examined 54 predetermined bacterial markers. We categorized patients according to the Montreal Classification and calculated the dysbiosis index (DI). Non-parametric tests were used to compare groups and the Bonferroni correction to adjust for multiple comparisons. RESULTS: The fluorescent signals (FSSs) for Firmicutes and Eubacterium hallii were lower in inflammatory bowel disease (IBD) vs. symptomatic controls (p<.05). FSS for Firmicutes, Lachnospiraceae, Eubacterium hallii and Ruminococcus albus/bromii were lower, whereas the signal for Bacteroides Fragilis was higher in UC vs. symptomatic controls (p<.05). FSS was higher for Bifidobacterium spp., Eubacterium hallii, Actinobacteria and Firmicutes among patients with ulcerative proctitis, compared to extensive colitis (p<.05). In CD, we observed no association with disease location. The DI correlated with faecal-calprotectin in both CD and in UC (p<.001). In terms of treatment escalation and anti-TNF response, differences were observed for some bacterial markers, but none of these associations were statistically significant. CONCLUSION: Our data reveal that the GA-map™ Dysbiosis Test holds the potential to characterize the faecal microbiota composition and to assess the degree of dysbiosis in new-onset IBD. On the other hand, our results cannot demonstrate any proven diagnostic or predictive value of this method to support clinical decision making.
Authors: Natalia Molinero; Diego Taladrid; Irene Zorraquín-Peña; Miguel de Celis; Ignacio Belda; Alex Mira; Begoña Bartolomé; M Victoria Moreno-Arribas Journal: Curr Issues Mol Biol Date: 2022-03-30 Impact factor: 2.976
Authors: Lena Öhman; Anders Lasson; Anna Strömbeck; Stefan Isaksson; Marcus Hesselmar; Magnus Simrén; Hans Strid; Maria K Magnusson Journal: Sci Rep Date: 2021-04-21 Impact factor: 4.379
Authors: Simen Svendsen Vatn; Jonas Christoffer Lindstrøm; Aina E F Moen; Stephan Brackmann; Tone M Tannæs; Christine Olbjørn; Daniel Bergemalm; Åsa V Keita; Fernando Gomollon; Trond Espen Detlie; Torben Lüders; Rahul Kalla; Alex Adams; Jack Satsangi; Jørgen Jahnsen; Morten H Vatn; Jonas Halfvarson; Petr Ricanek; Hilde Nilsen Journal: Clin Exp Gastroenterol Date: 2022-02-11