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Journal of Clinical Microbiology, November 2006, p. 4136-4141, Vol. 44, No. 11
0095-1137/06/$08.00+0     doi:10.1128/JCM.01004-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Differences between Tissue-Associated Intestinal Microfloras of Patients with Crohn's Disease and Ulcerative Colitis{triangledown} ,{ddagger}

Uri Gophna,1* Katrin Sommerfeld,2 Sharon Gophna,2,{dagger} W. Ford Doolittle,2 and Sander J. O. Veldhuyzen van Zanten3

Department of Molecular Microbiology and Biotechnology, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 69978, Israel,1 Genome Atlantic and Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia, Canada,2 Department of Medicine, Queen Elizabeth II Health Sciences Center, Dalhousie University, Halifax, Nova Scotia, Canada3

Received 15 May 2006/ Returned for modification 17 July 2006/ Accepted 8 September 2006

A leading hypothesis for the role of bacteria in inflammatory bowel diseases is that an imbalance in normal gut flora is a prerequisite for inflammation. Testing this hypothesis requires comparisons between the microbiota compositions of ulcerative colitis and Crohn's disease patients and those of healthy individuals. In this study, we obtained biopsy samples from patients with Crohn's disease and ulcerative colitis and from healthy controls. Bacterial DNA was extracted from the tissue samples, amplified using universal bacterial 16S rRNA gene primers, and cloned into a plasmid vector. Insert-containing colonies were picked for high-throughput sequencing, and sequence data were analyzed, yielding species-level phylogenetic data. The clone libraries yielded 3,305 sequenced clones, representing 151 operational taxonomical units. There was no significant difference between floras from inflamed and healthy tissues from within the same individual. Proteobacteria were significantly (P = 0.0007) increased in Crohn's disease patients, as were Bacteroidetes (P < 0.0001), while Clostridia were decreased in that group (P < 0.0001) in comparison with the healthy and ulcerative colitis groups, which displayed no significant differences. Thus, the bacterial flora composition of Crohn's patients appears to be significantly altered from that of healthy controls, unlike that of ulcerative colitis patients. Imbalance in flora in Crohn's disease is probably not sufficient to cause inflammation, since microbiotas from inflamed and noninflamed tissues were of similar compositions within the same individual.

* Corresponding author. Mailing address: Department of Molecular Microbiology and Biotechnology, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 69978, Israel. Phone: 972-3-6409988. Fax: 972-3-6409407. E-mail: urigo{at}tauex.tau.ac.il.

{triangledown} Published ahead of print on 20 September 2006.

{ddagger} Supplemental material for this article may be found at http://jcm.asm.org/.

{dagger} Present address: Department of Education, Tel Aviv, Israel.

Journal of Clinical Microbiology, November 2006, p. 4136-4141, Vol. 44, No. 11
0095-1137/06/$08.00+0     doi:10.1128/JCM.01004-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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