Abstract
Background
Background
Gut microbial composition has been proposed to influence disease onset in children with food protein–induced enterocolitis syndrome (FPIES).
Objective
We sought to investigate differences in gut microbiota profiles in children with newly diagnosed FPIES and healthy control subjects.
We sought to investigate differences in gut microbiota profiles in children with newly diagnosed FPIES and healthy control subjects.
Methods
Fecal samples were collected at FPIES diagnosis from 56 children stratified into 3 age groups: mean (SD) age 4.6 (0.5) months, 6.5 (0.6) months, and 11.7 (7.8) months. Gut microbiota profiles were analyzed using 16S ribosomal RNA gene amplicon sequencing and compared between children with FPIES and 43 age-matched control subjects.
Fecal samples were collected at FPIES diagnosis from 56 children stratified into 3 age groups: mean (SD) age 4.6 (0.5) months, 6.5 (0.6) months, and 11.7 (7.8) months. Gut microbiota profiles were analyzed using 16S ribosomal RNA gene amplicon sequencing and compared between children with FPIES and 43 age-matched control subjects.
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| Graphical Abstract |
Age was the strongest determinant of gut microbiota composition, followed by FPIES status. β-diversity differed significantly between children with FPIES and control subjects (P < .01), primarily driven by shifts in Bacteroidota, Proteobacteria, Actinobacteriota, and Verrucomicrobiota. Children with FPIES had lower Bifidobacterium and higher abundances of Bacteroides, Haemophilus, and Veillonella. FPIES food triggers were associated with reduced Verrucomicrobiota abundance.
Conclusions
Children with FPIES exhibit gut microbial dysbiosis characterized by reduced Bifidobacterium and Verrucomicrobiota abundance, suggesting potential links between early-life microbiota development and disease pathogenesis.
Children with FPIES exhibit gut microbial dysbiosis characterized by reduced Bifidobacterium and Verrucomicrobiota abundance, suggesting potential links between early-life microbiota development and disease pathogenesis.


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