LOOKING BEYOND THE ESOPHAGUS: INVESTIGATING THE INTESTINAL MICROBIOTA AND INFLAMMATION IN CHILDREN WITH REPAIRED ESOPHAGEAL ATRESIA
Isabelle Traini*1, Jessica Menzies2, Jennifer Hughes3, Tamarah Katz2, Michael J. Coffey1,4, Chee Y. Ooi1,5, Steven T. Leach1, Usha Krishnan1,5, EARTH Research Group on behalf of the1
1School of Women’s and Children’s Health, University of New South Wales, Sydney, New South Wales, Australia; 2Department of Nutrition and Dietetics, Sydney Children’s Hospital, Randwick, New South Wales, Australia; 3Department of Speech Pathology, Sydney Children’s Hospital, Randwick, New South Wales, Australia; 4Sydney Children’s Hospital, Randwick, New South Wales, Australia; 5Department of Gastroenterology, Sydney Children’s Hospital, Randwick, New South Wales, Australia
Background and Aim: There is limited literature exploring the intestinal microbiota and inflammation of children with repaired Esophageal Atresia (EA), which may contribute to their poor nutritional status. This study aimed to i) compare the intestinal microbiota and inflammation of children with EA to healthy controls (HC) and ii) correlate these factors with anthropometric measures.
Methods: Children with EA and HC from a single center in Sydney, Australia were recruited. Length/height-for-age, weight-for-age and weight-for-length/body-mass-index(BMI)-for-age z scores were calculated. Participants provided stool samples. The intestinal microbiota was analyzed using 16S rRNA sequencing (V4 region), and intestinal inflammation was measured using fecal calprotectin. Statistical analysis was performed using RStudio (v3.5.2). p<0.05 and q<0.05 (Benjamini-Hochberg correction) were considered significant.
Results: 35 children with EA and 35 matched HC were recruited (40% female), with a mean (SD) age of 6.3 (4.9) and 6.7 (5.0), respectively (p=0.68). Stool samples from 28 EA children and 28 HC matched for age and gender were analyzed using 16S rRNA sequencing. Alpha diversity analysis revealed that compared to HC, children with EA had significantly lower Shannon index (mean [SD] 3.42 [0.73] vs 2.94 [1.05] respectively, p=0.003) (Figure 1). Beta diversity analysis (relative abundance Bray-Curtis dissimilarities) revealed clustering between EA and HC cohorts (R2=0.03, p=0.04). There were several differences in the relative abundance of bacterial taxa between EA and HC cohorts (Table 1). Correlations between bacterial taxa and anthropometric z-scores in children with EA identified positive correlations between weight-for-length/BMI-for-age z scores and the genus Leptotrichia (rs=0.87, q<0.05). Fecal calprotectin was measured in 35 EA and 35 matched HC samples, and was higher in EA children compared to HC (median [IQR] 151.5 [68.1-371.1] vs 49.3 [19.1-97.6] mg/kg respectively, p=2.3x10-6). Spearman correlations between microbiota and calprotectin revealed significant (q<0.01) correlations between calprotectin and Ruminiclostridium (rs=-0.73), Faecalibacterium (rs=-0.70) and Enterobacter (rs=0.70) in the EA cohort. There was a negative correlation between calprotectin and length/height-for-age z scores in the EA cohort, which approached significance (rs=-0.33, p=0.066).
Conclusion: Children with EA have an altered intestinal microbiota compared to HC, which may contribute to intestinal inflammation and poor nutritional status. Further exploration of the clinical implications of these findings and the role of potential microbiota-modulating therapeutics in the EA cohort is warranted.
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