DIVERSITY OF HUMAN MILK OLIGOSACCHARIDE METABOLIZING GENES IN TWO INFANT COHORTS - DIVERSITY OF HUMAN MILK OLIGOSACCHARIDE METABOLIZING GENES IN TWO INFANT COHORTS Project Summary Atopic dermatitis/eczema is a growing problem in the United States and affects nearly 20% of infants. It usually begins during the first six months of an infant’s life. Early atopy is also one of the predictors of later allergic or other hyperinflammatory health problems. Observational studies have demonstrated a protective effect of human milk feeding for atopic dermatitis/eczema in infants. Thus, to protect their child from this disease, some women choose to feed their infants human milk. However, there is conflicting evidence on the effectiveness of this intervention. Although diet is likely an important contributor to this disease, the composition of the microbiota and its ability to digest a specific component of the diet is potentially just as important in protecting against atopic dermatitis/eczema. In fact, the ability of the intestinal microbiota to metabolize specific human milk oligosaccharides (HMOs) may explain why human milk feeding protects against atopic dermatitis/eczema in some but not all infants fed human milk. In this project, we will investigate microbial metabolism and metabolic products and identify their association to atopic dermatitis. More specifically, we will assess the taxonomic, functional, and metabolic composition of gut-resident bacteria from hundreds of infants residing in the Midwest or Northeast United States to determine the diversity, prevalence, and abundance of microbial HMO metabolism. This multi-omic data will be linked to reports of atopic dermatitis/eczema in the respective infants. We may also identify microbiota-associated genes or metabolites that are protective against atopic dermatitis/eczema. We expect that infants with a more diverse repertoire of HMO metabolizing genes present in their gut microbiome will be protected from atopic dermatitis/eczema. Performing this research in two different regions of the US will be especially advantageous, since subtle differences in medical or cultural practices, or simply geographic differences in microbial exposure, may alter HMO metabolizing gene repertoires independent of breastfeeding behavior. This research will dramatically improve our understanding of microbial HMO metabolism in human infants in the United States and determine whether a specific pattern of HMO metabolizing genes protects infants from atopic dermatitis and eczema.
