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      Role of Cytokine-Induced Glycosylation Changes in Regulating Cell Interactions and Cell Signaling in Inflammatory Diseases and Cancer

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          Abstract

          Glycosylation is one of the most important modifications of proteins and lipids, and cell surface glycoconjugates are thought to play important roles in a variety of biological functions including cell-cell and cell-substrate interactions, bacterial adhesion, cell immunogenicity and cell signaling. Alterations of glycosylation are observed in number of diseases such as cancer and chronic inflammation. In that context, pro-inflammatory cytokines have been shown to modulate cell surface glycosylation by regulating the expression of glycosyltransferases involved in the biosynthesis of carbohydrate chains. These changes in cell surface glycosylation are also known to regulate cell signaling and could contribute to disease pathogenesis. This review summarizes our current knowledge of the glycosylation changes induced by pro-inflammatory cytokines, with a particular focus on cancer and cystic fibrosis, and their consequences on cell interactions and signaling.

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          Most cited references127

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          Origin and physiological roles of inflammation.

          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
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            Colorectal cancer in mice genetically deficient in the mucin Muc2.

            The gastrointestinal tract is lined by a layer of mucus comprised of highly glycosylated proteins called mucins. To evaluate the importance of mucin in intestinal carcinogenesis, we constructed mice genetically deficient in Muc2, the most abundant secreted gastrointestinal mucin. Muc2-/- mice displayed aberrant intestinal crypt morphology and altered cell maturation and migration. Most notably, the mice frequently developed adenomas in the small intestine that progressed to invasive adenocarcinoma, as well as rectal tumors. Thus, Muc2 is involved in the suppression of colorectal cancer.
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              Experimental models of inflammatory bowel disease.

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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Cells
                Cells
                cells
                Cells
                MDPI
                2073-4409
                29 November 2016
                December 2016
                : 5
                : 4
                : 43
                Affiliations
                [1 ]Structural and Functional Glycobiology Unit, UMR CNRS 8576, University of Lille, Villeneuve d’Ascq 59655, France; justine.dewald@ 123456etudiant.univ-lille1.fr (J.H.D.); sophie.groux-degroote@ 123456univ-lille1.fr (S.G.-D.)
                [2 ]Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GE, UK; florent.colomb@ 123456liverpool.ac.uk
                [3 ]Institut Européen de Génomique du Diabète (EGID), Centre hospitalier universitaire (CHU) de Lille, Institut Pasteur de Lille, Institut national de la santé et de la recherche médicale (INSERM) U1011, University of Lille, Lille 59000, France; marie.bobowski@ 123456hotmail.fr
                Author notes
                [* ]Correspondence: philippe.delannoy@ 123456univ-lille1.fr ; Tel.: +33-320-436-923
                Article
                cells-05-00043
                10.3390/cells5040043
                5187527
                27916834
                1a9cfadc-cf78-4756-bd6d-7bbbf84a0321
                © 2016 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 14 October 2016
                : 24 November 2016
                Categories
                Review

                cytokines,glycosylation,glycosyltransferases,o-glycans,mucins,gangliosides,rtks,cell signaling,sialyl-lewisx

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