IL-31RA and TRPV1 Expression in Atopic Dermatitis Induced with Trinitrochlorobenzene in Nc/Nga Mice

Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Interleukin 31 (IL-31), a novel cytokine in AD, causes pruritus, typically characteristic of AD patients. The transient receptor potential vanilloid type 1 (TRPV1) is a cation channel activated by diverse noxious stimuli that has...

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Published in:International journal of molecular sciences 2023-09, Vol.24 (17), p.13521
Main Authors: Lee, Seokwoo, Lim, Na Yeon, Kang, Min Soo, Jeong, Yunho, Ahn, Jin-Ok, Choi, Jung Hoon, Chung, Jin-Young
Format: Article
Language:English
Subjects:
Advertising executives
Allergens
Allergies
Analysis
Atopic dermatitis
Communication
Cytokines
Dermatitis
Eczema
Edema
Erythema
Hyperplasia
Immune system
Inflammation
Interleukins
Kinases
Medical research
Medicine, Experimental
Pathogenesis
Pruritus
Skin
Skin diseases
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Summary:Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Interleukin 31 (IL-31), a novel cytokine in AD, causes pruritus, typically characteristic of AD patients. The transient receptor potential vanilloid type 1 (TRPV1) is a cation channel activated by diverse noxious stimuli that has been studied in a variety of pruritic skin diseases. In this study, the AD animal model was generated by administering the hapten, trinitrochlorobenzene (TNCB), to Nc/Nga mice, and the degree of expression of the IL-31 receptor alpha (IL-31RA) and TRPV1 in the skin of these atopic models was evaluated. The Nc/Nga mice were divided into 3 groups: control, TNCB 2-weeks treated, and TNCB 8-weeks treated. After inducing AD, the skin lesions in each group were scored and compared, and the histology of the skin lesions and the IL-31RA and TRPV1 expression for each group were evaluated by analyzing immunohistochemistry. The results show a significant difference in the skin lesion scores between the groups. The immunohistochemistry evaluation highlighted the remarkable expression of IL-31RA and TRPV1 in the nerve fibers of the TNCB 8-weeks-treated group. We thus confirmed that the long-term application of TNCB induced chronic atopic-like dermatitis and that IL-31RA and TRPV1 were overexpressed in the peripheral nerve fibers in this AD model.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms241713521