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      S100A4 contributes to colitis development by increasing the adherence of Citrobacter rodentium in intestinal epithelial cells

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          Abstract

          S100A4 has been implicated in cancer and several inflammatory diseases, but its role in inflammatory bowel disease has not been well investigated. Here, upon infection with Citrobacter rodentium, a model for enteropathogenic Escherichia coli infection in humans, induced the infiltration of a large number of S100A4 + cells into the colon in wild type (WT) mice. Deficiency of S100A4 reduced weight loss, bacterial colonization and colonic pathology. Furthermore, the expression of inflammatory cytokines and the recruitment of macrophages and neutrophils also decreased significantly in S100A4 knock out ( S100A4 −/−) mice. In vitro, soluble S100A4 directly up-regulated expression of integrin β−1 in intestinal epithelial cells and significantly increased the adherence of C. rodentium to intestinal epithelial cells. Additionally, the effects of S100A4 on the adherence of C. rodentium to epithelial cells could be abolished by a receptor for advanced glycation end products (RAGE)-specific inhibitor (FPS-ZM1). Therefore, these data indicate a novel mechanism for S100A4 that promotes colitis development by enhancing host adhesion and colonization of Citrobacter rodentium through the S100A4-mediated host inflammatory responses.

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          Most cited references43

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          Diarrheagenic Escherichia coli.

          Escherichia coli is the predominant nonpathogenic facultative flora of the human intestine. Some E. coli strains, however, have developed the ability to cause disease of the gastrointestinal, urinary, or central nervous system in even the most robust human hosts. Diarrheagenic strains of E. coli can be divided into at least six different categories with corresponding distinct pathogenic schemes. Taken together, these organisms probably represent the most common cause of pediatric diarrhea worldwide. Several distinct clinical syndromes accompany infection with diarrheagenic E. coli categories, including traveler's diarrhea (enterotoxigenic E. coli), hemorrhagic colitis and hemolytic-uremic syndrome (enterohemorrhagic E. coli), persistent diarrhea (enteroaggregative E. coli), and watery diarrhea of infants (entero-pathogenic E. coli). This review discusses the current level of understanding of the pathogenesis of the diarrheagenic E. coli strains and describes how their pathogenic schemes underlie the clinical manifestations, diagnostic approach, and epidemiologic investigation of these important pathogens.
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            Metal chelation and inhibition of bacterial growth in tissue abscesses.

            Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.
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              Citrobacter rodentium: infection, inflammation and the microbiota.

              Citrobacter rodentium is a mucosal pathogen of mice that shares several pathogenic mechanisms with enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E. coli (EHEC), which are two clinically important human gastrointestinal pathogens. Thus, C. rodentium has long been used as a model to understand the molecular basis of EPEC and EHEC infection in vivo. In this Review, we discuss recent studies in which C. rodentium has been used to study mucosal immunology, including the deregulation of intestinal inflammatory responses during bacteria-induced colitis and the role of the intestinal microbiota in mediating resistance to colonization by enteric pathogens. These insights should help to elucidate the roles of mucosal inflammatory responses and the microbiota in the virulence of enteric pathogens.
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                Author and article information

                Contributors
                zhangjh@bjtu.edu.cn
                xuexiangb@aliyun.com
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                21 September 2017
                21 September 2017
                2017
                : 7
                : 12099
                Affiliations
                [1 ]ISNI 0000 0004 1789 9622, GRID grid.181531.f, College of Life Science and Bioengineering, Beijing Jiaotong University, ; Beijing, 100044 P.R. China
                [2 ]ISNI 0000 0004 1789 9163, GRID grid.27446.33, School of Life Sciences, Northeast Normal University, ; Changchun, 130024 P.R. China
                [3 ]ISNI 0000 0004 0627 1442, GRID grid.458488.d, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, ; Beijing, 100101 P.R. China
                [4 ]State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, 100193 P. R. China
                Author information
                http://orcid.org/0000-0001-8957-8893
                Article
                12256
                10.1038/s41598-017-12256-z
                5608709
                28935867
                49404af0-aea6-4d14-b785-a74b4434acdb
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 28 March 2017
                : 5 September 2017
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