ILEAL AND COLONIC MUCOSAL MICROBIOTA IN DOGS WITH STEROID RESPONSIVE CHRONIC ENTEROPATHY

Exact aetiology for inflammatory chronic enteropathies in dogs remains unknown. Accumulating evidence suggests a pivotal role for intestinal dysbiosis in disease pathogenesis. Many studies have evaluated the alteration of faecal microbiota in canine chronic gastrointestinal (GI) disease, and less research is focused on mucosal microbiota, especially in the ileum and colon. The objectives of the current study were to evaluate ileal and colonic mucosal microbiota in dogs with steroid responsive enteropathy (SRE) before and after 4 months of treatment, and to compare them to control dogs (CD). A total of 10 dogs diagnosed with SRE were enrolled. Complete GI endoscopy was performed and samples were collected by a cytology brush at diagnosis (SRE-Baseline, n = 10) and after 4 month of treatment (SRE-After, n = 8). Oral laxative and 2–4 water enemas were performed before endoscopy. A total of 6 CD that were euthanized for reasons unrelated to this study, with no GI disease, were included. Samples from CD were obtained during necropsy within 3 hours of death. Mucosal genomic DNA was extracted and used for Illumina sequencing of 16S rRNA genes. Sequence data were analysed using the QIIME pipeline. Statistical significance was set at P < 0.05. Clinical signs improved significantly after 4 month of treatment in SRE, but no improvement was seen on endoscopic or histological evaluation. Significant differences in microbial communities between SRE-baseline and CD were observed in the colon (ANOSIM P = 0.002), but not in the ileum (ANOSIM P = 0.180). In dogs with SRE, both ileal and colonic microbial communities remained similar after 4 month of treatment (ANOSIM P = 0.189 and P = 0.637, respectively), and were different from CD (ANOSIM P = 0.001 and P = 0.004, respectively). Results of this study suggest that the mucosal microbiota in the colon of dogs with SRE is different from that of CD. Although clinical signs improved, colonic mucosal dysbiosis was still present after 4 months of treatment.