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Aryl hydrocarbon receptor expression in serum,peripheral blood mononuclear cells,and skin lesions of patients with atopic dermatitis and its correlation with disease severity 被引量:8

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摘要 Background:The aryl hydrocarbon receptor(AhR)is a ligand-activated transcription factor,which is critically involved in the pathogenesis of a variety of skin diseases.The aim of this study was to detect AhR and its downstream regulators including cytochrome P450(CYP1A1),AhR nuclear translocation(ARNT),and aryl hydrocarbon receptor repressor(AhRR)in serum,peripheral blood mononuclear cells(PBMCs),and skin lesions in patients with atopic dermatitis(AD).Methods:Twenty-nine AD patients defined according to the criteria of Hanifin and Rajka and Chinese criteria of AD were included.Subjects without allergic and chronic diseases were recruited as controls.Patients and controls were selected from the dermatology outpatient clinic of Peking University People’s Hospital from August 1 to December 31 in 2018.Enzyme-linked immunosorbent assay was performed to detect serum AhR level.ThemRNA of AhR,AhRR,ARNT,and CYP1A1 in PBMCs were measured by realtime quantitative polymerase chain reaction.AhR expression in skin lesions was measured by immunohistochemistry.Results:AhR was significantly higher expressed in serum(41.26±4.52 vs.33.73±2.49 pmol/L,t=6.507,P<0.001)and skin lesions(0.191±0.041 vs.0.087±0.017,t=10.036,P<0.001)of AD patients compared with those of controls.The mRNA levels of AhR(1.572±0.392 vs.1.000±0.173,t=6.819,P<0.001),AhRR(2.402±1.716 vs.1.000±0.788,t=3.722,P<0.001),CYP1A1(2.258±1.598 vs.1.000±0.796,t=3.400,P=0.002)in PBMCs of AD patients were higher compared with those of controls.The difference in mRNA levels of ARNT was not statistically significant between the patients and controls(1.383±0.842 vs.1.000±0.586,t=1.653,P=0.105).AhR mRNA levels in PBMCs positively correlated with eczema area and severity index score and serum interleukin-6 levels.Conclusion:AhR and its downstream regulators were highly expressed in serum,PBMCs,and skin of AD patients,which might contribute to the pathogenesis of AD.
出处 《Chinese Medical Journal》 SCIE CAS CSCD 2020年第2期148-153,共6页 中华医学杂志(英文版)
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