UNDERSTANDING HOST-MICROBIAL INTERACTIONS THAT PREDISPOSE INFANTS TO ATOPIC DERMATITIS

Abstract

<h3>Introduction</h3> The development of Atopic Dermatitis (AD) is largely multi factorial. This study utilized multi-omic analyses to determine the complex network of host immunological and microbial interactions in AD. <h3>Methods</h3> 125 term infants were included in this longitudinal cohort study. Infants were dichotomized as AD (n=35) or non-AD (n=90) based on parental responses on the Infant Feeding Practice survey at 1,4,6,12 months (confirmed with review of medical records). At 6 months, saliva was collected for analysis of microRNAs, cytokines, and microbial RNA. AD severity was assessed with the Scoring Atopic Dermatitis (SCORAD) tool. <h3>Results</h3> One cytokine ratio, two microRNA (miR-375-3p, miR-21-5p) and one bacterial phylum differed between groups (p < 0.05). The ratio of Th1 and Th2 cytokines (IL-8/IL6) was higher (d = 0.33, p = 0.041) among infants with AD. Levels of miR-375-3p were lower (d = -0.50, p = 0.009), and miR-21-5p were higher among infants with AD (d = 0.37, p = 0.007). Alpha diversity of bacterial RNA expression (Simpson index) was higher among infants with AD (d = 0.61, p = 0.001). Proteobacteria was positively correlated with miR-375-3p (R = 0.32, p = 0.017). Additionally, AD severity was positively correlated with Proteobacteria levels (R = 0.21, p = 0.010). <h3>Conclusion</h3> Elevated levels of pathogenic Proteobacteria may directly induce inflammatory cytokines. Alternatively, Proteobacteria may elicit host microRNA responses, which impacts production of IL-6 and IL-8. Therefore, host immunological and microbial predispositions may influence the pro-inflammatory environment in AD.