Toxicological Research

  • 제34권1호
  • /
  • Pages.7-12
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  • 2018
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  • 1976-8257(pISSN)
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  • 2234-2753(eISSN)
한국독성학회 (Korean Society of Toxicology & Korea Environmental Mutagen Society)
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Molecular Mechanism of Atopic Dermatitis Induction Following Sensitization and Challenge with 2,4-Dinitrochlorobenzene in Mouse Skin Tissue

  • Kim, JiYoun (Department of Occupational Health, Catholic University of Daegu) ;
  • Lee, JaeHee (Department of Occupational Health, Catholic University of Daegu) ;
  • Shin, SoJung (Department of Occupational Health, Catholic University of Daegu) ;
  • Cho, AhRang (Department of Occupational Health, Catholic University of Daegu) ;
  • Heo, Yong (Department of Occupational Health, Catholic University of Daegu)
  • 투고 : 2017.09.19
  • 심사 : 2017.10.20
  • 발행 : 2018.01.15
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초록

Laboratory animal models have been developed to investigate preventive or therapeutic effect of medicinal products, or occurrence or progression mechanism of atopic dermatitis (AD), a pruritic and persistent inflammatory skin disease. The murine model with immunologic phenomena resembling human AD was introduced, which demonstrated skewedness toward predominance of type-2 helper T cell reactivity and pathophysiological changes similar as human AD following 2,4-dinitrochlorobenzene (DNCB) sensitization and challenge. Molecular mechanism on the DNCB-mediated AD was further evaluated. Skin tissues were collected from mice treated with DNCB, and each tissue was equally divided into two sections; one for protein and the other for mRNA analysis. Expression of filaggrin, an important protein for keratinocyte integrity, was evaluated through SDS-PAGE. Level of mRNA expression for cytokines was determined through semi-quantitative reverse transcriptase polymerase chain reaction. Expression of filaggrin protein was significantly enhanced in the mice treated with DNCB compared with the vehicle (acetone : olive oil = 4 : 1 mixture) treatment group or the normal group without any treatment. Level of tumor necrosis factor-alpha and interleukin-18 mRNA expression, cytokines involved in activity of type-1 helper T ($T_H1$) cell, was significantly downregulated in the AD group compared with other control groups. These results suggest that suppression of $T_H1$ cell-mediated immune response could be reflected into the skin tissue of mice treated with DNCB for AD induction, and disturbance of keratinocyte integrity might evoke a compensatory mechanism.

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참고문헌

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피인용 문헌

  1. IL-1α and IL-1β as alternative biomarkers for risk assessment and the prediction of skin sensitization potency vol.81, pp.17, 2018, https://doi.org/10.1080/15287394.2018.1494474