Kansal S^1,2,3, Catto-Smith AG^3,4, Boniface K², Thomas S², Cameron DJ¹, Oliver M¹, Alex G¹, Kirkwood CD^2,5, Wagner J^3,6. J Pediatr Gastroenterol Nutr. 2019 Aug 6. doi: 10.1097/MPG.0000000000002461. [Epub ahead of print]

Author information

1 Department of Gastroenterology and Clinical Nutrition, Royal Children's Hospital, Parkville, Victoria, Australia.

2 Enteric Virus group, Murdoch Children's Research Institute, Parkville, Victoria, Australia.

3 Department of Pediatrics, University of Melbourne, Parkville, Victoria, Australia.

4 Department of Gastroenterology, Hepatology and Liver Transplant, Lady Cilento Children's Hospital, Brisbane, Queensland, Australia.

5 Enteric and Diarrheal Diseases, Global Health, Bill and Melinda Gates Foundation, Seattle, Washington, USA.

6 Wellcome Trust, Sanger Institute, Cambridge, UK.

Abstract

OBJECTIVES: Crohn's Disease (CD) is a chronic relapsing condition possibly caused by a dysbiotic microbiome. About 30-60% of CD patients have antibodies to Saccharomyces cerevisiae (ASCA), but any association with gut microbiota is unexplored. We hypothesized that ASCA positivity would predict a signature microbial status and clinical phenotype.

METHODS: Ileocolonic mucosal biopsies were obtained from children with CD (n?=?135), and controls without inflammatory boweldisease (n?=?45). Comparison was made between ASCA status, microbial diversity and clinical characteristics.

RESULTS: ASCA was highly specific but poorly sensitive for the diagnosis of CD. In patients with CD, ASCA positivity was associated with older age (≥10 years), ileocolonic disease and long-term risk of surgery. Microbial alpha and beta diversity were similar in CD patients with or without ASCA, but significantly less when compared to non-IBD controls. Microbial richness was similar across all three groups. Fourteen bacterial species were associated with ASCA positive CD patients and 14 species with ASCA negative patients (p?

CONCLUSION: ASCA positive and ASCA negative CD patients have significant differences in gut microbiome composition, which could possibly be influencing the phenotype of the disease.