Abstract

BackgroundPrevious 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.MethodsSpot 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.ResultsFecal 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).ConclusionsAn 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.

Highlights

  • Previous data suggest that fecal S100A12 protein (S100A12) has clinical utility as a biomarker of chronic gastrointestinal inflammation in both people and dogs, but the effect of gastrointestinal pathogens on fecal S100A12 concentrations is largely unknown

  • The S100A12 protein is a ligand for the pattern recognition receptor receptor of advanced glycation end products (RAGE) and activates the nuclear factor kappa B (NFkB) pathway [6, 14], a mechanism linked to the pathogenesis of autoimmune disorders such as inflammatory bowel disease (IBD) in humans [6, 15, 16]

  • This study showed that fecal S100A12 concentrations in puppies are not affected by an infection with Toxocara canis or Giardia sp

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Summary

Introduction

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 difficult to study in traditional animal models due to the lack of S100A12 expression in rodents. 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. The S100A12 protein is a ligand for the pattern recognition receptor RAGE (receptor for advanced glycation end products) and activates the nuclear factor kappa B (NFkB) pathway [6, 14], a mechanism linked to the pathogenesis of autoimmune disorders such as inflammatory bowel disease (IBD) in humans [6, 15, 16]

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