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Background: The infant fecal microbiome is known to impact subsequent asthma risk, but the environmental exposures impacting this association, the role of the maternal microbiome, and how the microbiome impacts different childhood asthma phenotypes are unknown. Methods: Our objective was to identify associations between features of the prenatal and early‐life fecal microbiomes and child asthma phenotypes. We analyzed fecal 16 s rRNA microbiome profiling and fecal metabolomic profiling from stool samples collected from mothers during the third trimester of pregnancy (n = 120) and offspring at ages 3–6 months (n = 265), 1 (n = 436) and 3 years (n = 506) in a total of 657 mother–child pairs participating in the Vitamin D Antenatal Asthma Reduction Trial. We used clinical data from birth to age 6 years to characterize subjects with asthma as having early, transient or active asthma phenotypes. In addition to identifying specific genera that were robustly associated with asthma phenotypes in multiple covariate‐adjusted models, we clustered subjects by their longitudinal microbiome composition and sought associations between fecal metabolites and relevant microbiome and clinical features. Results: Seven maternal and two infant fecal microbial taxa were robustly associated with at least one asthma phenotype, and a longitudinal gut microenvironment profile was associated with early asthma (Fisher exact test p =.03). Though mode of delivery was not directly associated with asthma, we found substantial evidence for a pathway whereby cesarean section reduces fecal Bacteroides and microbial sphingolipids, increasing susceptibility to early asthma. Conclusion: Overall, our results suggest that the early‐life, including prenatal, fecal microbiome modifies risk of asthma, especially asthma with onset by age 3 years. [ABSTRACT FROM AUTHOR]

Here, using data from the Canadian CHILD Cohort Study, we performed a sex-stratified analysis of human milk adiponectin, leptin, and insulin concentrations and their association with possible or probable asthma development by 3 years of age. For this analysis, asthma was classified as "possible or probable asthma" or "no asthma." Milk hormone concentrations did not differ in milk produced for sons vs. daughters (Table, Figure A); however, sex-specific associations were observed between milk hormone concentrations and child asthma (Table, Figure B). It is known that circulating leptin can stimulate the production of pro-inflammatory cytokines, potentially mediating the asthma-obesity axis; however, it is not known whether leptin in human milk can trigger similar responses. [Extracted from the article]

In contrast to other environmental allergens, the association with atopic dermatitis was present for Fel d 1, which may suggest that the skin is an important route of sensitization for this allergen. GLO:1X5/01dec19:all13927-fig-0002.jpg PHOTO (COLOR): Hierarchical clustering performed on patient sensitization profiles and allergen components indicating clusters by allergen source and biochemical family (sensitized: N = 37; nonsensitized: N = 18). In conclusion, we provide data describing a potentially high-risk preschool asthma cohort in Canada using a comprehensive approach capturing sensitization to allergens of paramount importance. By applying both allergen extracts and components, we identified that peanut and animal allergens from cat and dog were major allergen sources in this North American cohort of preschool asthmatics. [Extracted from the article]