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Nat Rev Gastroenterol Hepatol. 2014 Oct;11(10):588-600. doi: 10.1038/nrgastro.2014.78. Epub 2014 Jun 10.

The role of glycosylation in IBD.

Author information

Centre for Population Health Sciences, University of Edinburgh, Teviot Place, EH8 9AG, Edinburgh, UK.
Centre for Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, Edinburgh, UK.
Department of Biomolecular Systems, Max Planck Institute of Colloids and Interfaces, Am Mühlenberg 1 OT Golm, 14476, Potsdam, Germany.
Genos Ltd, Hondlova 2, 10000 Zagreb, Croatia.
University of Zagreb, Faculty of Science, Horvatovac 102a, 10000 Zagreb, Croatia.
Ludger Ltd, Culham Science Centre, Oxford, OX14 3EB, UK.
IP Research Consulting SAS, 34 Rue Carnot, 93160 Noisy-le-Grand, Paris, France.
Center for Proteomics and Metabolomics, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, Netherlands.
Department of Medical and Surgical Specialities, Division of Gastroenterology, AOU Careggi University Hospital, Largo Brambilla 13, 50139 Florence, Italy.
F.Widjaja Family Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Suite D4063, Los Angeles, CA 90048, USA.
Department of Biochemistry and Molecular Biology, University of Zagreb Faculty of Pharmacy and Biochemistry, Trg maršala Tita 14, 10000 Zagreb, Croatia.


A number of genetic and immunological studies give impetus for investigating the role of glycosylation in IBD. Experimental mouse models have helped to delineate the role of glycosylation in intestinal mucins and to explore the putative pathogenic role of glycosylation in colitis. These experiments have been extended to human studies investigating the glycosylation patterns of intestinal mucins as well as levels of glycans of serum glycoproteins and expression of glycan receptors. These early human studies have generated interesting hypotheses regarding the pathogenic role of glycans in IBD, but have generally been restricted to fairly small underpowered studies. Decreased glycosylation has been observed in the intestinal mucus of patients with IBD, suggesting that a defective inner mucus layer might lead to increased bacterial contact with the epithelium, potentially triggering inflammation. In sera, decreased galactosylation of IgG has been suggested as a diagnostic marker for IBD. Advances in glycoprofiling technology make it technically feasible and affordable to perform high-throughput glycan pattern analyses and to build on previous work investigating a much wider range of glycan parameters in large numbers of patients.

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