843 Gene-environment interaction effects of AKR1C3 and particulate matter exposure in atopic eczema
نویسندگان
چکیده
The etiology of atopic eczema (AE) is complex and involves genetic as well environmental factors. Chronic exposure to airborne particulate matter (PM) contributes the development worsening AE. Biological effects PM are mainly initiated by surface-bound polycyclic aromatic hydrocarbons (PAH). Previous data our laboratory indicate that stimulating cutaneous aryl hydrocarbon receptor activity downstream expression aldo-keto reductase (AKR) 1C3, PAH may enforce 11-ketoreduction mast cell-derived prostaglandin (PG) D2, a metabolically unstable stimulator Th2 cells, 9α,11β-PGF2, stable inducer proatopic responses. To assess clinical relevance AKR1C3 for PM-related AE, we focused on single nucleotide polymorphism (SNP) in coding region gene conducted gene-environment interaction study. Specifically, using from cohort study, tested between SNP rs12529 with an aerodynamic diameter ≤2.5, ≤10, 2.5-10μm land-use regression models AE adjusted logistic analyses. We observed significant effect exposures adolescents. interacts PM2.5 (p-valueint=0.037), PM10 (p-valueint=0.019) PMcoarse (p-valueint=0.036). elucidate whether affects enzyme activity, next generated AKR1C3-deficient keratinocytes transiently transfected them constructs wild-type polymorph (point-mutated) AKR1C3. PGD2 treatment subsequent LC-MS based analyses 9α,11β-PGF2 formation revealed enhances activity. Our strongly worsen symptoms enforcing AKR1C3-mediated production Th2-stimulatory 9α,11β-PGF2.
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ژورنال
عنوان ژورنال: Journal of Investigative Dermatology
سال: 2022
ISSN: ['1523-1747', '0022-202X']
DOI: https://doi.org/10.1016/j.jid.2022.05.857