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Fecal Microbial Community Profiling Allows Discrimination of Phenotype and Treatment Response in Pediatric Crohn's
Denise Aldrian1, Adam Pollio2, Christoph Mayerhofer1
1Department of Paediatrics I, Medical University of Innsbruck, Innsbruck, Austria.
Insights
Pediatric inflammatory bowel disease (PIBD) involves altered gut microbiomes in both active and inactive stages. These microbial changes can serve as biomarkers for diagnosing PIBD subtypes and predicting treatment effectiveness.
Area of Science:
- Microbiome research
- Pediatric gastroenterology
- Inflammatory Bowel Disease (IBD)
Background:
- The exact causes of pediatric inflammatory bowel disease (PIBD), including Crohn's disease (CD) and ulcerative colitis (UC), remain unclear.
- Gut microbiome dysregulation is implicated in PIBD development and presents a potential therapeutic avenue.
Purpose of the Study:
- To systematically analyze gut microbiome composition in PIBD.
- To evaluate the potential of gut microbiome as a biomarker for disease progression and treatment response in children.
Main Methods:
- Systematic literature search of bibliographic and nucleotide databases.
- Analysis of 16S-rRNA sequencing data using a dada2/phyloseq pipeline.
- Extraction and analysis of patient metadata from 26 studies (3956 stool samples).
Main Results:
- Reduced alpha diversity in treatment-naïve PIBD patients compared to healthy controls, correlating with disease activity.
- Altered beta diversity indicating distinct microbial community structures in treatment-naïve and even in-remission PIBD patients.
- Machine learning models achieved high accuracy (AUROC 98%) in differentiating CD and UC in treatment-naïve children.
- Microbial communities differed between treatment responders and non-responders, with high accuracy (AUROC 82%-90%) in predicting response to specific therapies.
Conclusions:
- Gut microbial community structure is significantly altered in children with PIBD, irrespective of disease activity.
- Microbiome profiling shows promise as a biomarker for distinguishing PIBD subtypes.
- Gut microbiome analysis can aid in predicting patient response to various treatments.
Background And Aims:
The pathophysiology of pediatric inflammatory bowel disease (PIBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), is not entirely understood. Dysregulation of the intestinal microbiome is recognized as both a disease-driving and a potential therapeutic target. This study aimed to systematically analyze gut microbiome compositions and its applicability as a biomarker for disease progress and treatment response.
Methods:
Bibliographic and nucleotide databases were searched. Raw 16S-rRNA sequencing reads were subjected to a uniform downstream dada2/phyloseq pipeline to extract taxonomy, community structure, and abundance information. Patient metadata were extracted from publications, and study authors were contacted for further details if required.
Results:
Twenty-six studies comprising 3956 stool samples (CD 41%, UC 36%, 23% healthy) were included in the analyses. Median age of individuals was 12 (interquartile range 4). Sex distribution was comparable. Alpha diversity was reduced between the healthy and both UC and CD treatment-naïve groups (P < .001) and further reduced with increasing clinical disease activity. Beta diversity revealed altered community structure in treatment-naïve children with PIBD (P < .001). This alteration remained in patients in clinical remission (P < .001). Machine learning models discriminated between treatment-naïve patients with CD or UC with an area under the receiver operating characteristics curve (AUROC) of 98%. Microbial communities differed between patient responders versus nonresponders to treatment (P < .001). Further, microbial community profiling distinguished treatment response (eg, steroid, nutrition, or TNFα) with AUROCs of 82%-90%.
Conclusions:
Gut microbial community structure is substantially altered in active and inactive PIBD and may be utilized as a biomarker for differentiating PIBD subtype and predicting treatment response.
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