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      Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

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          Abstract

          Background

          Adiponectin, a protein hormone produced by adipose tissues, exhibits anti-inflammatory functions in various models. This study was investigated the effects of adiponectin on dextran sodium sulfate (DSS)-colonic injury, inflammation, apoptosis, and intestinal barrier dysfunction in Caco-2 cell and mice.

          Materials and methods

          The results showed that DSS caused inflammatory response and intestinal barrier dysfunction in vitro and in vivo. Adiponectin injection alleviated colonic injury and rectal bleeding in mice. Meanwhile, adiponectin downregulated colonic IL-1β and TNF-α expressions and regulated apoptosis relative genes to attenuate DSS-induced colonic inflammation and apoptosis. Adiponectin markedly reduced serum lipopolysaccharide concentration, a biomarker for intestinal integrity, and enhanced colonic expression of tight junctions (ZO-1 and occludin). The in vitro data further demonstrated that adiponectin alleviated DSS-induced proinflammatory cytokines production and the increased permeability in Caco-2 cells.

          Conclusion

          Adiponectin plays a beneficial role in DSS-induced inflammation via alleviating apoptosis and improving intestinal barrier integrity.

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          Most cited references42

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          Intestinal barrier in inflammatory bowel disease.

          Lena Antoni, Sabine Nuding, Jan Wehkamp … (2014)
          A complex mucosal barrier protects as the first line of defense the surface of the healthy intestinal tract from adhesion and invasion by luminal microorganisms. In this review, we provide an overview about the major components of this protective system as for example an intact epithelium, the synthesis of various antimicrobial peptides (AMPs) and the formation of the mucus layer. We highlight the crucial importance of their correct functioning for the maintenance of a proper intestinal function and the prevention of dysbiosis and disease. Barrier disturbances including a defective production of AMPs, alterations in thickness or composition of the intestinal mucus layer, alterations of pattern-recognition receptors, defects in the process of autophagy as well as unresolved endoplasmic reticulum stress result in an inadequate host protection and are thought to play a crucial role in the pathogenesis of the inflammatory bowel diseases Crohn's disease and ulcerative colitis.
          Article 0 comments Cited 160 times – based on 0 reviews     Review now
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            The role of macrophages and dendritic cells in the initiation of inflammation in IBD.

            Erin C Steinbach, Scott E. Plevy (2014)
            In the healthy gastrointestinal tract, homeostasis is an active process that requires a careful balance of host responses to the enteric luminal contents. Intestinal macrophages and dendritic cells (DCs) comprise a unique group of tissue immune cells that are ideally situated at the interface of the host and the enteric luminal environment to appropriately respond to microbes and ingested stimuli. However, intrinsic defects in macrophage and DC function contribute to the pathogenesis of inflammatory bowel diseases, as highlighted by recent genome-wide association studies. Gastrointestinal macrophages and DCs participate in inflammatory bowel disease development through inappropriate responses to enteric microbial stimuli, inefficient clearance of microbes from host tissues, and impaired transition from appropriate proinflammatory responses to anti-inflammatory responses that promote resolution. By understanding how intestinal macrophages and DCs initiate chronic inflammation, new pathogenesis-based therapeutic strategies to treat human inflammatory bowel diseases will be elucidated.
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              Role of the intestinal barrier in inflammatory bowel disease.

              Mike Laukoetter, Porfirio Nava, Asma Nusrat (2008)
              A critical function of the intestinal mucosa is to form a barrier that separates luminal contents from the interstitium. The single layer of intestinal epithelial cells (IECs) serves as a dynamic interface between the host and its environment. Cell polarity and structural properties of the epithelium is complex and is important in the development of epithelial barrier function. Epithelial cells associate with each other via a series of intercellular junctions. The apical most intercellular junctional complex referred to as the Apical Junction Complex (AJC) is important in not only cell-cell recognition, but also in the regulation of paracellular movement of fluid and solutes. Defects in the intestinal epithelial barrier function have been observed in a number of intestinal disorders such as inflammatory bowel disease (IBD). It is now becoming evident that an aberrant epithelial barrier function plays a central role in the pathophysiology of IBD. Thus, a better understanding of the intestinal epithelial barrier structure and function in healthy and disease states such as IBD will foster new ideas for the development of therapies for such chronic disorders.
              Article 0 comments Cited 80 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Xiuli Zuo: zuoxiuli_s@163.com
                Journal
                Journal ID (nlm-ta): Inflamm Res
                Journal ID (iso-abbrev): Inflamm. Res
                Title: Inflammation Research
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 1023-3830
                ISSN (Electronic): 1420-908X
                Publication date (Electronic): 15 May 2018
                Publication date PMC-release: 15 May 2018
                Publication date (Print): 2018
                Volume: 67
                Issue: 8
                Pages: 663-670
                Affiliations
                [1 ]Department of Gastroenterology, Taian City Central Hospital, Taian, Shandong People’s Republic of China
                [2 ]Department of Medicine, Beijing 316 Hospital, Beijing, People’s Republic of China
                [3 ]Department of Cerebral Surgery, Taian City Central Hospital, Taian, Shandong People’s Republic of China
                [4 ]Department of Stomatology, Taian City Central Hospital, Taian, Shandong People’s Republic of China
                [5 ]ISNI 0000 0004 1761 1174, GRID grid.27255.37, Department of Gastroenterology, Qilu Hospital, , Shandong University, ; 107 Wenhua West Road, Jinan, 250012 People’s Republic of China
                Author notes

                Responsible Editor: John Di Battista.

                Article
                Publisher ID: 1155
                DOI: 10.1007/s00011-018-1155-6
                PMC ID: 6028846
                PubMed ID: 29766204
                SO-VID: b657271f-06fe-4f54-8c63-ae556ea0bb0e
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 11 April 2018
                Date revision received : 27 April 2018
                Date accepted : 3 May 2018
                Categories
                Subject: Original Research Paper
                Custom metadata
                issue-copyright-statement © Springer International Publishing AG, part of Springer Nature 2018

                ScienceOpen disciplines: Immunology
                Keywords: adiponectin,inflammation,apoptosis,barrier
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: adiponectin, inflammation, apoptosis, barrier

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