Skin Treatment with Detergent Induces Dermatitis with H1-Antihistamine-Refractory Itch and Upregulates IL-4 and Th17/Th22 Cytokine Gene Expression in C57BL/6 Mice
| Autor: | Yurie Masutani, Toshiro Takai, Seiji Kamijo, Toru Kimitsu, Tomoko Yoshimura, Saori Ichikawa, Saya Shimizu, Takasuke Ogawa, Keiko Takada, Mitsutoshi Tominaga, Hajime Suto, Kenji Takamori, Hideoki Ogawa, Ko Okumura, Shigaku Ikeda |
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| Rok vydání: | 2022 |
| Předmět: |
Inflammation
Pruritus Immunology Detergents Interleukin-17 Sodium Histamine Antagonists Gene Expression Water Dermatitis Forkhead Transcription Factors General Medicine T-Lymphocytes Helper-Inducer Nuclear Receptor Subfamily 1 Group F Member 3 Mice Inbred C57BL Mice Irritants Immunology and Allergy Animals Cytokines Interleukin-4 Skin |
| Zdroj: | International archives of allergy and immunology. 183(10) |
| ISSN: | 1423-0097 |
| Popis: | Introduction: Repeated skin contact to detergents causes chronic irritant contact dermatitis (ICD) associated with itch sensation and eczema. However, the mechanisms of detergent-induced ICD are poorly understood. Here, we established a new murine model of detergent-induced ICD with H1-antihistamine-refractory itch. Methods: Ear skin of wild-type and mast cell-deficient mice on the C57BL/6 genetic background was treated with a detergent, sodium dodecyl/lauryl sulfate (SDS), daily for approximately 2 weeks with or without administration of an H1-antihistamine, fexofenadine. Skin inflammation, barrier dysfunction, and itching were analyzed. Quantitative PCR for earlobe gene expression and flow cytometry analysis for draining lymph node cells were conducted. Results: SDS treatment induced skin inflammation with ear swelling, increased transepidermal water loss, and hind-paw scratching behaviors in the wild-type and mast cell-deficient mice. The peak value of scratching bouts was retained for at least 48 h after the last SDS treatment. H1-antihistamine administration showed no or little reduction in the responses. SDS treatment upregulated gene expression for a Th2 cytokine IL-4 and Th17/Th22 cytokines, IL-17A, IL-17F, and IL-22, and increased cell numbers in draining lymph nodes of CD4+ T, CD8+ T, and γδT cells with enhanced expression of GATA3, RORγt, T-bet, or FOXP3 compared with untreated mice. Conclusions: The present study showed that SDS treatment of ear skin in C57BL/6 mice induces mast cell-independent skin inflammation with H1-antihistamine-refractory itch and suggested a possible Th cytokine- and/or lymphocyte-mediated regulation of the model. The model would be useful for elucidation of mechanisms for inflammation with H1-antihistamine-refractory itch in detergent-induced ICD. |
| Databáze: | OpenAIRE |
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