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      Effect of selected gastrointestinal parasites and viral agents on fecal S100A12 concentrations in puppies as a potential comparative model

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          Abstract

          Background

          Previous data suggest that fecal S100A12 has clinical utility as a biomarker of chronic gastrointestinal inflammation (idiopathic inflammatory bowel disease) in both people and dogs, but the effect of gastrointestinal pathogens on fecal S100A12 concentrations is largely unknown. The role of S100A12 in parasite and viral infections is also difficult to study in traditional animal models due to the lack of S100A12 expression in rodents. Thus, the aim of this study was to evaluate fecal S100A12 concentrations in a cohort of puppies with intestinal parasites ( Cystoisospora spp., Toxocara canis, Giardia sp.) and viral agents that are frequently encountered and known to cause gastrointestinal signs in dogs (coronavirus, parvovirus) as a comparative model.

          Methods

          Spot fecal samples were collected from 307 puppies [median age (range): 7 (4−13) weeks; 29 different breeds] in French breeding kennels, and fecal scores (semiquantitative system; scores 1−13) were assigned. Fecal samples were tested for Cystoisospora spp. ( C. canis and C. ohioensis), Toxocara canis, Giardia sp., as well as canine coronavirus (CCV) and parvovirus (CPV). S100A12 concentrations were measured in all fecal samples using an in-house radioimmunoassay. Statistical analyses were performed using non-parametric 2-group or multiple-group comparisons, non-parametric correlation analysis, association testing between nominal variables, and construction of a multivariate mixed model.

          Results

          Fecal S100A12 concentrations ranged from < 24−14,363 ng/g. Univariate analysis only showed increased fecal S100A12 concentrations in dogs shedding Cystoisospora spp. ( P = 0.0384) and in dogs infected with parvovirus ( P = 0.0277), whereas dogs infected with coronavirus had decreased fecal S100A12 concentrations ( P = 0.0345). However, shedding of any single enteropathogen did not affect fecal S100A12 concentrations in multivariate analysis (all P > 0.05) in this study. Only fecal score and breed size had an effect on fecal S100A12 concentrations in multivariate analysis ( P < 0.0001).

          Conclusions

          An infection with any single enteropathogen tested in this study is unlikely to alter fecal S100A12 concentrations, and these preliminary data are important for further studies evaluating fecal S100A12 concentrations in dogs or when using fecal S100A12 concentrations as a biomarker in patients with chronic idiopathic gastrointestinal inflammation.

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          Most cited references31

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          RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides.

          S100/calgranulin polypeptides are present at sites of inflammation, likely released by inflammatory cells targeted to such loci by a range of environmental cues. We report here that receptor for AGE (RAGE) is a central cell surface receptor for EN-RAGE (extracellular newly identified RAGE-binding protein) and related members of the S100/calgranulin superfamily. Interaction of EN-RAGEs with cellular RAGE on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Blockade of EN-RAGE/RAGE quenches delayed-type hypersensitivity and inflammatory colitis in murine models by arresting activation of central signaling pathways and expression of inflammatory gene mediators. These data highlight a novel paradigm in inflammation and identify roles for EN-RAGEs and RAGE in chronic cellular activation and tissue injury.
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            ASVCP reference interval guidelines: determination of de novo reference intervals in veterinary species and other related topics.

            Reference intervals (RI) are an integral component of laboratory diagnostic testing and clinical decision-making and represent estimated distributions of reference values (RV) from healthy populations of comparable individuals. Because decisions to pursue diagnoses or initiate treatment are often based on values falling outside RI, the collection and analysis of RV should be approached with diligence. This report is a condensation of the ASVCP 2011 consensus guidelines for determination of de novo RI in veterinary species, which mirror the 2008 Clinical Laboratory and Standards Institute (CLSI) recommendations, but with language and examples specific to veterinary species. Newer topics include robust methods for calculating RI from small sample sizes and procedures for outlier detection adapted to data quality. Because collecting sufficient reference samples is challenging, this document also provides recommendations for determining multicenter RI and for transference and validation of RI from other sources (eg, manufacturers). Advice for use and interpretation of subject-based RI is included, as these RI are an alternative to population-based RI when sample size or inter-individual variation is high. Finally, generation of decision limits, which distinguish between populations according to a predefined query (eg, diseased or non-diseased), is described. Adoption of these guidelines by the entire veterinary community will improve communication and dissemination of expected clinical laboratory values in a variety of animal species and will provide a template for publications on RI. This and other reports from the Quality Assurance and Laboratory Standards (QALS) committee are intended to promote quality laboratory practices in laboratories serving both clinical and research veterinarians. © 2012 American Society for Veterinary Clinical Pathology.
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              RAGE signaling sustains inflammation and promotes tumor development

              A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.
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                Author and article information

                Contributors
                romy.heilmann@kleintierklinik.uni-leipzig.de
                a.grellet@envt.fr
                niels.gruetzner@landw.uni-halle.de
                shannonmcranford@gmail.com
                jsuchodolski@cvm.tamu.edu
                s.chastant@envt.fr
                jsteiner@cvm.tamu.edu
                Journal
                Parasit Vectors
                Parasit Vectors
                Parasites & Vectors
                BioMed Central (London )
                1756-3305
                17 April 2018
                17 April 2018
                2018
                : 11
                : 252
                Affiliations
                [1 ]ISNI 0000 0001 2230 9752, GRID grid.9647.c, Small Animal Clinic, College of Veterinary Medicine, , University of Leipzig, ; An den Tierkliniken 23, DE-04103 Leipzig, Germany
                [2 ]ISNI 0000 0004 4687 2082, GRID grid.264756.4, Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, , Texas A&M University, ; 465 Raymond Stotzer Pkwy, College Station, TX 77843-4474 USA
                [3 ]ISNI 0000 0001 2353 1689, GRID grid.11417.32, NeoCare, IHAP, , University of Toulouse, ; INRA, ENVT, 23 chemin des Capelles, BP 87614, 31076 Toulouse Cedex 03, France
                [4 ]ISNI 0000 0001 0679 2801, GRID grid.9018.0, Institute of Agricultural and Nutritional Sciences, , Martin Luther University Halle-Wittenberg, ; Theodor-Lieser St 11, DE-06120 Halle (Saale), Germany
                Article
                2841
                10.1186/s13071-018-2841-5
                5905106
                29665827
                aa6d7182-5613-4c12-bfb4-26ff4417ab49
                © The Author(s). 2018

                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. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 11 December 2017
                : 9 April 2018
                Categories
                Research
                Custom metadata
                © The Author(s) 2018

                Parasitology
                biomarker,canine,calgranulin c,diarrhea,enteropathogen,parasite,virus
                Parasitology
                biomarker, canine, calgranulin c, diarrhea, enteropathogen, parasite, virus

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