Does canine inflammatory bowel disease influence gut microbial profile and host metabolism?

Jia Xu,Geert P J Janssens,Venessa Eeckhaut,Myriam Hesta,Isabel Van De Maele,Filip Van Immerseel,Tom Van De Wiele,Guido Bosch,Yufeng Niu,Marta Lourenço,Adronie Verbrugghe,Daisy J X Liu,Brigitte Wuyts,Greet Junius

doi:10.1186/s12917-016-0736-2

Abstract

BackgroundInflammatory bowel disease (IBD) refers to a diverse group of chronic gastrointestinal diseases, and gut microbial dysbiosis has been proposed as a modulating factor in its pathogenesis. Several studies have investigated the gut microbial ecology of dogs with IBD but it is yet unclear if this microbial profile can alter the nutrient metabolism of the host. The aim of the present study was to characterize the faecal bacterial profile and functionality as well as to determine host metabolic changes in IBD dogs.Twenty-three dogs diagnosed with IBD and ten healthy control dogs were included. Dogs with IBD were given a clinical score using the canine chronic enteropathy clinical activity index (CCECAI). Faecal short-chain fatty acids (SCFA) and ammonia concentrations were measured and quantitative PCR was performed. The concentration of plasma amino acids, acylcarnitines, serum folate, cobalamin, and indoxyl sulfate was determined.ResultsNo significant differences in the abundance of a selection of bacterial groups and fermentation metabolites were observed between the IBD and control groups. However, significant negative correlations were found between CCECAI and the faecal proportion of Lactobacillus as well as between CCECAI and total SCFA concentration. Serum folate and plasma citrulline were decreased and plasma valine was increased in IBD compared to control dogs. Increased plasma free carnitine and total acylcarnitines were observed in IBD compared with control dogs, whereas short-chain acylcarnitines (butyrylcarnitine + isobutyrylcarnitine and, methylmalonylcarnitine) to free carnitine ratios decreased. Dogs with IBD had a higher 3-hydroxyisovalerylcarnitine + isovalerylcarnitine to leucine ratio compared to control dogs.ConclusionsCanine IBD induced a wide range of changes in metabolic profile, especially for the plasma concentrations of short-chain acylcarnitines and amino acids, which could have evolved from tissue damage and alteration in host metabolism. In addition, dogs with more severe IBD were characterised by a decrease in faecal proportion of Lactobacillus.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-016-0736-2) contains supplementary material, which is available to authorized users.

Highlights

Inflammatory bowel disease (IBD) refers to a diverse group of chronic gastrointestinal diseases, and gut microbial dysbiosis has been proposed as a modulating factor in its pathogenesis
IBD has been associated with a decrease in butyrate-producing bacteria including the major butyrate producing bacteria, clostridial cluster IV and XIVa, Faecalibacterium prausnitzii, and the terminal gene to produce butyrate, butyryl-co-enzyme A (CoA) acetate-CoA transferase (BCoAT) gene [8,9,10]
Faecal microbiota No differences were found between IBD and control dogs for the relative abundance of Firmicutes, Bacteroidetes, Enterobacteriaceae, Lactobacillus, clostridial cluster I, IV and XIVa in faecal samples, nor for the number of gene copies of butyryl-CoA acetate-CoA transferase (BCoAT) and dissimilative sulphate-reducing bacteria gene (q > 0.05) (Table 2)

Summary

Introduction

Inflammatory bowel disease (IBD) refers to a diverse group of chronic gastrointestinal diseases, and gut microbial dysbiosis has been proposed as a modulating factor in its pathogenesis. The aim of the present study was to characterize the faecal bacterial profile and functionality as well as to determine host metabolic changes in IBD dogs. Canine idiopathic inflammatory bowel disease (IBD) is a group of disorders characterized by persistent or recurrent clinical signs of gastro-intestinal disease of undetermined cause associated with histological evidence of inflammation in the small or large intestinal mucosa [1]. IBD has been associated with a decrease in butyrate-producing bacteria including the major butyrate producing bacteria, clostridial cluster IV and XIVa, Faecalibacterium prausnitzii, and the terminal gene to produce butyrate, butyryl-CoA acetate-CoA transferase (BCoAT) gene [8,9,10].

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