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Inflamm Bowel Dis. 2015 Aug;21(8):1948-56. doi: 10.1097/MIB.0000000000000454.

Fungal Signature in the Gut Microbiota of Pediatric Patients With Inflammatory Bowel Disease.

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*Division of Gastroenterology, Perelman School of Medicine, The University of Pennsylvania, Philadelphia, Pennsylvania; †Department of Microbiology, Perelman School of Medicine, The University of Pennsylvania, Philadelphia, Pennsylvania; and ‡Division of Gastroenterology, Hepatology, and Nutrition, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.



Inflammatory bowel disease (IBD) involves dysregulation of mucosal immunity in response to environmental factors such as the gut microbiota. The bacterial microbiota is often altered in IBD, but the connection to disease is not fully clarified and gut fungi have recently been suggested to play a role as well. In this study, we compared microbes from all 3 domains of life-bacteria, archaea, and eukaryota-in pediatric patients with IBD and healthy controls.


A stool sample was collected from patients with IBD (n = 32) or healthy control subjects (n = 90), and bacterial, archaeal, and fungal communities were characterized by deep sequencing of rRNA gene segments specific to each domain.


Patients with IBD (Crohn's disease or ulcerative colitis) had lower bacterial diversity and distinctive fungal communities. Two lineages annotating as Candida were significantly more abundant in patients with IBD (P = 0.0034 and P = 0.00038, respectively), whereas a lineage annotating as Cladosporium was more abundant in healthy subjects (P = 0.0025). There were no statistically significant differences in archaea, which were rare in pediatric samples compared with those from adults.


Pediatric IBD is associated with reduced diversity in both fungal and bacterial gut microbiota. Specific Candida taxa were found to be increased in abundance in the IBD samples. These data emphasize the potential importance of fungal microbiota signatures as biomarkers of pediatric IBD, supporting their possible role in disease pathogenesis.

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