Analysis of Mucosal Microbiota in Inflammatory Bowel Disease using a Custom Phylogenetic Microarray
Journal: Austin Journal of Gastroenterology (Vol.1, No. 4)Publication Date: 2014-08-22
Authors : Arun Gupta; Seungha Kang; Josef Wagner; Carl Kirkwood; Mark Morrison; Chris McSweeney; Finlay Macrae;
Page : 1-6
Keywords : Microbiota; Microarray; Inflammatory bowel disease; Crohn’s disease; Ulcerative colitis;
Abstract
Background and Aims: The pathogenesis of inflammatory bowel disease is likely to involve interaction between genetic factors, innate immunity, and the enteric microbiota. Alterations in the composition of the normal commensal microbiota may play a pathogenic role. Methods: A custom 2240 probe oligonucleotide microarray based on 16s RNA sequences was used to compare the microbiota profiles of patients with inflammatory bowel disease with controls. Twenty mucosal samples obtained from colonoscopic biopsies were analysed - five from Crohn’s Disease Inflamed (CDI) tissue, five from Crohn’s Disease Non-Inflamed (CDNI), five from Ulcerative Colitis (UC), and five healthy control samples. Analysis was performed using principal components analysis and between group analysis. Results: The microbiota from both Crohn’s disease and ulcerative colitis differed significantly from the control group, though not between CDI and CDNI groups. Alterations in the abundance of Faecalibacterium prausnitzii, Shigella flexneri, Dorea longicatena, and Xenorhabdus bovienii were associated with Crohn’s disease. Alterations in the abundance of Yersinia pestis and Eubacterium rectale were associated with ulcerative colitis. Conclusion: The gastrointestinal microbiota differed in mucosal samples from patients with inflammatory bowel disease compared to those taken from controls. The composition of the microbiota was not altered by the presence of inflammation. The abundance of particular organisms including the previously described F. prausnitzii was found to be different in patients with inflammatory bowel disease compared to healthy controls, and new putative aetiological organisms were identified. These findings support the hypothesis that a bacterial ‘dysbiosis’ may contribute to the pathogenesis of inflammatory bowel disease.
Other Latest Articles
- Low Virulence of Helicobacter Pylori and Gastric Cancer: the Contribution of Polymorphisms of iNOS and DNA Repair Enzymes in this Process
- Clinical Course, Treatment Strategies, Social and Economic Impact of Ulcerative Colitis: An Overview
- Safety Profile of Anti-TNF Agents in Polish Pediatric Patients with Crohn’s Disease
- Splenosis Presenting as Pancreatic Neoplasm: Report of Two Cases
- A Unique Case Report of Solitary Transverse Colon Perforation in Behcet’s Disease
Last modified: 2016-06-24 20:15:12