Jessica H Savage1, Kathleen A Lee-Sarwar1, Joanne Sordillo2, Supinda Bunyavanich3,4, Yanjiao Zhou5,6,7, George O'Connor8, Megan Sandel9, Leonard B Bacharier10,11, Robert Zeiger12, Erica Sodergren5,7, George M Weinstock5,7, Diane R Gold13, Scott T Weiss13, Augusto A Litonjua13. 1. Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 2. Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care, Boston, MA, USA. 3. Department of Genetics and Genomic Sciences and Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 4. Division of Pediatric Allergy and Immunology, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 5. The Genome Institute at Washington University, St. Louis, MO, USA. 6. Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA. 7. The Jackson Laboratory for Genomic Medicine, Farmington, CT, USA. 8. Pulmonary Center and Department of Medicine, Boston University School of Medicine, Boston, MA, USA. 9. Department of Pediatrics, Boston Medical Center, Boston, MA, USA. 10. Division of Pediatric Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Washington University School of Medicine, St Louis, MO, USA. 11. St Louis Children's Hospital, St Louis, MO, USA. 12. Kaiser Permanente Southern California, San Diego, CA, USA. 13. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Abstract
BACKGROUND: Alterations in the intestinal microbiome are prospectively associated with the development of asthma; less is known regarding the role of microbiome alterations in food allergy development. METHODS: Intestinal microbiome samples were collected at age 3-6 months in children participating in the follow-up phase of an interventional trial of high-dose vitamin D given during pregnancy. At age 3, sensitization to foods (milk, egg, peanut, soy, wheat, walnut) was assessed. Food allergy was defined as caretaker report of healthcare provider-diagnosed allergy to the above foods prior to age 3 with evidence of IgE sensitization. Analysis was performed using Phyloseq and DESeq2; P-values were adjusted for multiple comparisons. RESULTS: Complete data were available for 225 children; there were 87 cases of food sensitization and 14 cases of food allergy. Microbial diversity measures did not differ between food sensitization and food allergy cases and controls. The genera Haemophilus (log2 fold change -2.15, P=.003), Dialister (log2 fold change -2.22, P=.009), Dorea (log2 fold change -1.65, P=.02), and Clostridium (log2 fold change -1.47, P=.002) were underrepresented among subjects with food sensitization. The genera Citrobacter (log2 fold change -3.41, P=.03), Oscillospira (log2 fold change -2.80, P=.03), Lactococcus (log2 fold change -3.19, P=.05), and Dorea (log2 fold change -3.00, P=.05) were underrepresented among subjects with food allergy. CONCLUSIONS: The temporal association between bacterial colonization and food sensitization and allergy suggests that the microbiome may have a causal role in the development of food allergy. Our findings have therapeutic implications for the prevention and treatment of food allergy.
BACKGROUND: Alterations in the intestinal microbiome are prospectively associated with the development of asthma; less is known regarding the role of microbiome alterations in food allergy development. METHODS: Intestinal microbiome samples were collected at age 3-6 months in children participating in the follow-up phase of an interventional trial of high-dose vitamin D given during pregnancy. At age 3, sensitization to foods (milk, egg, peanut, soy, wheat, walnut) was assessed. Food allergy was defined as caretaker report of healthcare provider-diagnosed allergy to the above foods prior to age 3 with evidence of IgE sensitization. Analysis was performed using Phyloseq and DESeq2; P-values were adjusted for multiple comparisons. RESULTS: Complete data were available for 225 children; there were 87 cases of food sensitization and 14 cases of food allergy. Microbial diversity measures did not differ between food sensitization and food allergy cases and controls. The genera Haemophilus (log2 fold change -2.15, P=.003), Dialister (log2 fold change -2.22, P=.009), Dorea (log2 fold change -1.65, P=.02), and Clostridium (log2 fold change -1.47, P=.002) were underrepresented among subjects with food sensitization. The genera Citrobacter (log2 fold change -3.41, P=.03), Oscillospira (log2 fold change -2.80, P=.03), Lactococcus (log2 fold change -3.19, P=.05), and Dorea (log2 fold change -3.00, P=.05) were underrepresented among subjects with food allergy. CONCLUSIONS: The temporal association between bacterial colonization and food sensitization and allergy suggests that the microbiome may have a causal role in the development of food allergy. Our findings have therapeutic implications for the prevention and treatment of food allergy.
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