We examined the fecal virome and bacterial community composition of children with Crohn disease (CD), ulcerative colitis (UC), and healthy controls to test the hypothesis that unique patterns of viral organisms and/or presence of bacterial pathogens may be identified that could contribute to the pathogenesis of pediatric inflammatory bowel disease (IBD).
Fecal samples from 24 children (mean 12.2 years) with CD (n = 7) or UC (n = 5) and similar aged controls (n = 12) were processed to determine individual viromes. Viral sequences were identified through translated protein sequence similarity search. Bacterial microbiota were determined by sequencing of the V4 region of the 16S rRNA gene.
Only a few human viruses were detected, so virome analyses focused on bacterial viruses. The relative abundance of Caudovirales was greater than that of Microviridae phages in both IBD and healthy controls. Caudovirales phages were more abundant in CD (mean 80.8%) than UC (48.8%) (P = 0.05) but not controls. The richness of viral strains in Microviridae but not Caudovirales was higher in controls than CD (P = 0.05) but not UC cases. No other measure of phage abundance, richness, or Shannon diversity showed significant difference between the 2 IBD and control groups. Bacterial microbiota analysis revealed that IBD diagnosis, albumin, hemoglobin, erythrocyte sedimentation rate, and probiotic supplementation correlated to the composition of gut bacterial microbiota.
Minor patterns in gut virome and bacterial community composition distinguish pediatric IBD patients from healthy controls. Probiotics are associated with bacterial microbiota composition. These exploratory results need confirmation in larger studies.
*Division of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, UCSF Benioff Children's Hospital, University of California, San Francisco
†Blood Systems Research Institute
‡Division of Gastroenterology, Department of Medicine
§Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA.
Address correspondence and reprint requests to Melvin B. Heyman, MD, Pediatric Gastroenterology/Nutrition, University of California, 550 16th St, 5th Floor, Mailstop 0136, San Francisco, CA 94143 (e-mail: email@example.com).
Received 27 April, 2018
Accepted 14 August, 2018
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Sources of support that require acknowledgment: Blood Systems Research Institute for support to T.G.P., X.D., and E.D. Funded in part by NIH Grant T32DK007762 (M.A.F. and S.G.V.) and by generous support from donors to the UCSF Pediatric IBD Research and Education Fund.
The authors report no conflicts of interest.