Antti E Seppo1, Kevin Bu2, Madina Jumabaeva1, Juilee Thakar3, Rakin A Choudhury3, Chloe Yonemitsu4, Lars Bode4,5, Camille A Martina6, Maria Allen7, Sabrina Tamburini2, Enrica Piras2, David S Wallach2, R John Looney7, Jose C Clemente2, Kirsi M Järvinen1,8. 1. Division of Allergy and Immunology, Center for Food Allergy, Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Golisano Children's Hospital, Rochester, New York, USA. 2. Department of Genetics and Genomic Sciences, Icahn Institute for Data Science and Genomic Technology, Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York City, NY, USA. 3. Department of Microbiology and Immunology and Department of Biostatistics, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA. 4. Division of Neonatology and Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of California San Diego, La Jolla, California, USA. 5. Mother-Milk-Infant Center of Research Excellence (MOMI CORE), University of California, San Diego, La Jolla, California, USA. 6. Department of Public Health & Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA. 7. Division of Allergy, Immunology, and Rheumatology, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA. 8. Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.
Abstract
BACKGROUND: Growing up on traditional, single-family farms is associated with protection against asthma in school age, but the mechanisms against early manifestations of atopic disease are largely unknown. We sought determine the gut microbiome and metabolome composition in rural Old Order Mennonite (OOM) infants at low risk and Rochester, NY urban/suburban infants at high risk for atopic diseases. METHODS: In a cohort of 65 OOM and 39 Rochester mother-infant pairs, 101 infant stool and 61 human milk samples were assessed by 16S rRNA gene sequencing for microbiome composition and qPCR to quantify Bifidobacterium spp. and B. longum ssp. infantis (B. infantis), a consumer of human milk oligosaccharides (HMOs). Fatty acids (FAs) were analyzed in 34 stool and human 24 milk samples. Diagnoses and symptoms of atopic diseases by 3 years of age were assessed by telephone. RESULTS: At a median age of 2 months, stool was enriched with Bifidobacteriaceae, Clostridiaceae, and Aerococcaceae in the OOM compared with Rochester infants. B. infantis was more abundant (p < .001) and prevalent, detected in 70% of OOM compared with 21% of Rochester infants (p < .001). Stool colonized with B. infantis had higher levels of lactate and several medium- to long/odd-chain FAs. In contrast, paired human milk was enriched with a distinct set of FAs including butyrate. Atopic diseases were reported in 6.5% of OOM and 35% of Rochester children (p < .001). CONCLUSION: A high rate of B. infantis colonization, similar to that seen in developing countries, is found in the OOM at low risk for atopic diseases.
BACKGROUND: Growing up on traditional, single-family farms is associated with protection against asthma in school age, but the mechanisms against early manifestations of atopic disease are largely unknown. We sought determine the gut microbiome and metabolome composition in rural Old Order Mennonite (OOM) infants at low risk and Rochester, NY urban/suburban infants at high risk for atopic diseases. METHODS: In a cohort of 65 OOM and 39 Rochester mother-infant pairs, 101 infant stool and 61 human milk samples were assessed by 16S rRNA gene sequencing for microbiome composition and qPCR to quantify Bifidobacterium spp. and B. longum ssp. infantis (B. infantis), a consumer of human milk oligosaccharides (HMOs). Fatty acids (FAs) were analyzed in 34 stool and human 24 milk samples. Diagnoses and symptoms of atopic diseases by 3 years of age were assessed by telephone. RESULTS: At a median age of 2 months, stool was enriched with Bifidobacteriaceae, Clostridiaceae, and Aerococcaceae in the OOM compared with Rochester infants. B. infantis was more abundant (p < .001) and prevalent, detected in 70% of OOM compared with 21% of Rochester infants (p < .001). Stool colonized with B. infantis had higher levels of lactate and several medium- to long/odd-chain FAs. In contrast, paired human milk was enriched with a distinct set of FAs including butyrate. Atopic diseases were reported in 6.5% of OOM and 35% of Rochester children (p < .001). CONCLUSION: A high rate of B. infantis colonization, similar to that seen in developing countries, is found in the OOM at low risk for atopic diseases.
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