Fecal microbiota in pediatric inflammatory bowel disease and its relation to inflammation

KL Kolho, K Korpela, T Jaakkola… - Official journal of the …, 2015 - journals.lww.com
KL Kolho, K Korpela, T Jaakkola, MVA Pichai, EG Zoetendal, A Salonen, WM De Vos
Official journal of the American College of Gastroenterology| ACG, 2015journals.lww.com
OBJECTIVES: Inflammatory bowel disease (IBD) is considered to result from interplay
between host and intestinal microbiota. While IBD in adults has shown to be associated with
marked changes in the intestinal microbiota, there are only a few studies in children, and
particularly studies focusing on therapeutic responses are lacking. Hence, this prospective
study addressed the intestinal microbiota in pediatric IBD especially related to the level of
inflammation. METHODS: In total, 68 pediatric patients with IBD and 26 controls provided …
Abstract
OBJECTIVES:
Inflammatory bowel disease (IBD) is considered to result from interplay between host and intestinal microbiota. While IBD in adults has shown to be associated with marked changes in the intestinal microbiota, there are only a few studies in children, and particularly studies focusing on therapeutic responses are lacking. Hence, this prospective study addressed the intestinal microbiota in pediatric IBD especially related to the level of inflammation.
METHODS:
In total, 68 pediatric patients with IBD and 26 controls provided stool and blood samples in a tertiary care hospital and 32 received anti-tumor necrosis factor-α (anti-TNF-α). Blood inflammatory markers and fecal calprotectin levels were determined. The intestinal microbiota was characterized by phylogenetic microarray and qPCR analysis.
RESULTS:
The microbiota varied along a gradient of increasing intestinal inflammation (indicated by calprotectin levels), which was associated with reduced microbial richness, abundance of butyrate producers, and relative abundance of Gram-positive bacteria (especiallyClostridiumclusters IV and XIVa). A significant association between microbiota composition and inflammation was indicated by a set of bacterial groups predicting the calprotectin levels (area under curve (AUC) of 0.85). During the induction of anti-TNF-α, the microbial diversity and similarity to the microbiota of controls increased in the responder group by week 6, but not in the non-responders (P< 0.01; response related to calprotectin levels). The abundance of six groups of bacteria including those related toEubacterium rectaleandBifidobacteriumspp. predicted the response to anti-TNF-α medication.
CONCLUSIONS:
Intestinal microbiota represents a potential biomarker for correlating the level of inflammation and therapeutic responses to be further validated.
Lippincott Williams & Wilkins