Articles On Atopic Dermatits

Atopic dermatitis (AD) may be a complex multifactorial inflammatory disease of the skin that affects ~280 million people worldwide. About 85% of AD cases begin in childhood, a big portion of which may persist into adulthood. Moreover, a typical progression of youngsters with AD to allergy , asthma or rhinitis has been reported (“allergic march” or “atopic march”). AD comprises highly heterogeneous sub-phenotypes/endotypes resulting from complex interplay between intrinsic and extrinsic factors, like environmental stimuli, and genetic factors regulating cutaneous functions (impaired barrier function, epidermal lipid, and protease abnormalities), immune functions and therefore the microbiome. Though the roles of high-throughput “omics” integrations in defining endotypes are recognized, current analyses are based on individual omics data and using binary clinical outcomes. Although individual omics analysis, like genome-wide association studies (GWAS), can effectively map variants correlated with AD, the bulk of the heritability and therefore the functional relevance of discovered variants aren't explained or known by the identified variants. The limited success of singular approaches underscores the necessity for holistic and integrated approaches to research complex phenotypes using trans-omics data integration strategies. Integrating omics layers (e.g., genome, epigenome, transcriptome, proteome, metabolome, lipidome, exposome, microbiome), which frequently have complementary and synergistic effects, might provide the chance to capture the flow of data underlying AD disease manifestation. Overlapping genes/candidates derived from multiple omics types include FLG, SPINK5, S100A8, and SERPINB3 in AD pathogenesis. Overlapping pathways include macrophage, endothelial cell and fibroblast activation pathways, additionally to well-known Th1/Th2 and NFkB activation pathways. Interestingly, there was more multi-omics overlap at the pathway level than gene level.      

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