Exposure to isocyanates predicts atopic dermatitis prevalence and disrupts therapeutic pathways in commensal bacteria

Atopic dermatitis (AD) is a chronic inflammatory skin condition increasing in industrial nations at a pace that suggests environmental drivers. We hypothesize that the dysbiosis associated with AD may signal microbial adaptations to modern pollutants. Having previously modeled the benefits of health-associated Roseomonas mucosa, we now show that R. mucosa fixes nitrogen in the production of protective glycerolipids and their cer-amide by-products. Screening EPA databases against the clinical visit rates identified diisocyanates as the stron-gest predictor of AD. Diisocyanates disrupted the production of beneficial lipids and therapeutic modeling for isolates of R. mucosa as well as commensal Staphylococcus. Last, while topical R. mucosa failed to meet commer-cial end points in a placebo-controlled trial, the subgroup who completed the full protocol demonstrated sus-tained, clinically modest, but statistically significant clinical improvements that differed by study site diisocyanate levels. Therefore, diisocyanates show temporospatial and epidemiological association with AD while also inducing eczematous dysbiosis.

Automated summary

Atopic dermatitis is a chronic inflammatory skin condition that is increasing in industrial nations, possibly due to environmental factors. The dysbiosis associated with atopic dermatitis may signal microbial adaptations to modern pollutants. R. mucosa has been found to fix nitrogen and produce protective glycerolipids and ceramide by-products, which can impact atopic dermatitis.