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      Fibrostenotic strictures in Crohn’s disease

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          Abstract

          The use of biologic agents including anti-tumor necrosis factor monoclonal antibodies followed by anti-integrins and anti-interleukins has drastically changed the treatment paradigm of Crohn’s disease (CD) by improving clinical symptoms and mucosal healing. However, up to 70% of CD patients still eventually undergo surgery mainly due to fibrostenotic strictures. There are no specific anti-fibrotic drugs yet. This review comprehensively addresses the mechanism, prediction, diagnosis and treatment of the fibrostenotic strictures in CD. We also introduce promising anti-fibrotic agents which may be available in the near future and summarize challenges in developing novel therapies to treat fibrostenotic strictures in CD.

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          Most cited references183

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          Pattern recognition receptors and inflammation.

          Osamu Takeuchi, Shizuo Akira (2010)
          Infection of cells by microorganisms activates the inflammatory response. The initial sensing of infection is mediated by innate pattern recognition receptors (PRRs), which include Toll-like receptors, RIG-I-like receptors, NOD-like receptors, and C-type lectin receptors. The intracellular signaling cascades triggered by these PRRs lead to transcriptional expression of inflammatory mediators that coordinate the elimination of pathogens and infected cells. However, aberrant activation of this system leads to immunodeficiency, septic shock, or induction of autoimmunity. In this Review, we discuss the role of PRRs, their signaling pathways, and how they control inflammatory responses. 2010 Elsevier Inc. All rights reserved.
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            Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease.

            J Hugot, M Chamaillard, H Zouali … (2001)
            Crohn's disease and ulcerative colitis, the two main types of chronic inflammatory bowel disease, are multifactorial conditions of unknown aetiology. A susceptibility locus for Crohn's disease has been mapped to chromosome 16. Here we have used a positional-cloning strategy, based on linkage analysis followed by linkage disequilibrium mapping, to identify three independent associations for Crohn's disease: a frameshift variant and two missense variants of NOD2, encoding a member of the Apaf-1/Ced-4 superfamily of apoptosis regulators that is expressed in monocytes. These NOD2 variants alter the structure of either the leucine-rich repeat domain of the protein or the adjacent region. NOD2 activates nuclear factor NF-kB; this activating function is regulated by the carboxy-terminal leucine-rich repeat domain, which has an inhibitory role and also acts as an intracellular receptor for components of microbial pathogens. These observations suggest that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-kB in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn's disease that can now be further investigated.
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              Smad-dependent and Smad-independent pathways in TGF-beta family signalling.

              Rik Derynck, Ying Zhang (2003)
              Transforming growth factor-beta (TGF-beta) proteins regulate cell function, and have key roles in development and carcinogenesis. The intracellular effectors of TGF-beta signalling, the Smad proteins, are activated by receptors and translocate into the nucleus, where they regulate transcription. Although this pathway is inherently simple, combinatorial interactions in the heteromeric receptor and Smad complexes, receptor-interacting and Smad-interacting proteins, and cooperation with sequence-specific transcription factors allow substantial versatility and diversification of TGF-beta family responses. Other signalling pathways further regulate Smad activation and function. In addition, TGF-beta receptors activate Smad-independent pathways that not only regulate Smad signalling, but also allow Smad-independent TGF-beta responses.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Intest Res
                Journal ID (iso-abbrev): Intest Res
                Journal ID (publisher-id): IR
                Title: Intestinal Research
                Publisher: Korean Association for the Study of Intestinal Diseases
                ISSN (Print): 1598-9100
                ISSN (Electronic): 2288-1956
                Publication date (Print): October 2020
                Publication date (Electronic): 10 April 2020
                Volume: 18
                Issue: 4
                Pages: 379-401
                Affiliations
                [1 ]Digestive Disease Center, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea
                [2 ]Department of Colorectal Surgery, Hepatology and Nutrition, Digestive Diseases and Surgery Institute, Cleveland Clinic Foundation, Cleveland, OH, USA
                [3 ]Department of Gastroenterology, Hepatology and Nutrition, Digestive Diseases and Surgery Institute, Cleveland Clinic Foundation, Cleveland, OH, USA
                Author notes
                Correspondence to Jun Hwan Yoo, Digestive Disease Center, CHA Bundang Medical Center, CHA University School of Medicine, 59 Yatap-ro, Bundanggu, Seongnam 13496, Korea. Tel: +82-31-780-4906, Fax: +82-31-780-5219, E-mail: jhyoo@ 123456cha.ac.kr
                Author information
                http://orcid.org/0000-0002-5810-4019
                http://orcid.org/0000-0002-2549-9042
                http://orcid.org/0000-0002-9087-1568
                Article
                Publisher ID: ir-2019-09148
                DOI: 10.5217/ir.2019.09148
                PMC ID: 7609387
                PubMed ID: 32259917
                SO-VID: 311a706a-b355-4d5b-9585-96889fc09b2b
                Copyright © © Copyright 2020. Korean Association for the Study of Intestinal Diseases. All rights reserved.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 12 November 2019
                Date revision received : 21 January 2020
                Date accepted : 26 January 2020
                Categories
                Subject: Review

                Keywords: crohn disease,stricture,fibrostenosis,intestinal fibrosis,endoscopic balloon dilatation
                Data availability:
                Keywords: crohn disease, stricture, fibrostenosis, intestinal fibrosis, endoscopic balloon dilatation

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