Intestinal microbiota is modified in pediatric food protein-induced enterocolitis syndrome

Esther Caparrós; María Carmen Cenit; Javier Muriel; Alfonso Benítez-Páez; María Victoria Moreno; Purificación González-Delgado; Gonzalo Rubio; Yolanda Sanz; Javier Fernández

doi:10.1016/j.jacig.2022.07.005

Intestinal microbiota is modified in pediatric food protein-induced enterocolitis syndrome

J Allergy Clin Immunol Glob. 2022 Sep 6;1(4):217-224. doi: 10.1016/j.jacig.2022.07.005. eCollection 2022 Nov.

Authors

Affiliations

¹ Clinical Medicine Department, University Miguel Hernández, San Juan de Alicante, Alicante, Spain.
² Microbial Ecology, Nutrition, and Health Research Unit, Institute of Agrochemistry and Food Technology, Paterna, Valencia, Spain.
³ Foundation for the Promotion of Sanitary and Biomedical Research of Valencian Community, Valencia, Spain.
⁴ Host-Microbe Interactions in Metabolic Health Laboratory, Principe Felipe Research Center, Valencia, Spain.
⁵ Allergy Service, Alicante General University Hospital, Alicante Institute for Health and Biomedical Research, Alicante, Spain.
⁶ Department of Biochemistry, Molecular Biology "B" and Immunology, University of Murcia, Murcia, Spain.

Abstract

Background: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated food hypersensitivity that affects the gastrointestinal system, especially in children, who often present with more severe clinical manifestations than adults do. Although its pathogenesis is poorly understood and biomarkers are still lacking, scientific evidence suggests that gut microbiota may play an important role in the development of FPIES.

Objective: We aimed to compare the composition of gut microbiota in children with FPIES with that in age- and sex-matched healthy controls.

Methods: We analyzed the gut microbiota profiles in fecal samples of 17 patients with FPIES (case patients) and 12 age-matched healthy children (controls) by tag sequencing of the 16S ribosomal RNA gene hypervariable V4-V5 regions. Subjects' sociodemographic, clinical, and food diary variables were described and compared between groups by using inferential statistical tests. Nonparametric linear discriminant analysis was performed for intestinal microbiota data.

Results: Patients with confirmed cases FPIES (n = 17; average patient age, 7.5 ± 3.2 years) and controls without FPIES or any atopy (n = 12, average patient age, 6.9 ± 2.7 years) were included. Fish was the main FPIES-inducing allergen in 65% of the cases. The patients with FPIES showed higher proportions of Lachnospiraceae spp (P < .0286) and a lower proportion of Ruminococcaceae spp (P < .0066), Lactobacillaceae spp (P < .0075), and Leuconostocaceae spp (P < .0173) than the controls.

Conclusions: Our data clearly show a different gut microbial signature in patients with FPIES, suggesting a new potential avenue for aiding the diagnosis and clinical management of FPIES. Larger studies are needed to confirm these results.

Keywords: FPIES; Lachnospiraceae; Lactobacillaceae; Leuconostocaceae; Ruminococcaceae; gut microbiota; microbiome; non–IgE-mediated food hypersensivity.