The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunction
Background: House dust mite (HDM) allergens can induce or exacerbate allergic inflammation, including atopic dermatitis (AD). Substances that damage the epithelial barrier can trigger or worsen AD. The mechanism by which the novel HDM allergen Der p 39 induces allergic inflammation remains unclear....
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| Language: | English |
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Elsevier
2025-03-01
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| Series: | World Allergy Organization Journal |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S1939455125000110 |
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| author | Shan Liu, BSc Ze-Lang Cai, MS Jingcheng Liu Si-Yi Que, BSc Wan-Zhen Hu, MS Liang Chen, MS Jia-Jie Chen, PhD Kunmei Ji, PhD |
| author_facet | Shan Liu, BSc Ze-Lang Cai, MS Jingcheng Liu Si-Yi Que, BSc Wan-Zhen Hu, MS Liang Chen, MS Jia-Jie Chen, PhD Kunmei Ji, PhD |
| author_sort | Shan Liu, BSc |
| collection | DOAJ |
| description | Background: House dust mite (HDM) allergens can induce or exacerbate allergic inflammation, including atopic dermatitis (AD). Substances that damage the epithelial barrier can trigger or worsen AD. The mechanism by which the novel HDM allergen Der p 39 induces allergic inflammation remains unclear. Our aim was to investigate the effects of Der p 39 on AD-like inflammation and associated mechanisms. Methods: Dinitrochlorobenzene (DNCB) and Der p 39 were utilized to establish AD model mice. Inflammation severity was evaluated with physiological and morphological assays. The effects of Der p 39 on inflammatory cytokine release and skin barrier protein expression were examined in HaCaT cells (human epidermal keratinocytes). Mitogen-activated protein kinase (MAPK) activation was examined by western blots. MAPK inhibitors were employed to assess MAPK involvement in filaggrin expression. Results: Der p 39 worsened allergic inflammation (tissue thickness) in murine ears pretreated with 1% DNCB. Compared to controls, Der p 39-sensitized tissues showed epidermal and dermal thickening with elevated numbers of mast cells and eosinophils in inflammatory lesions. Der p 39 increased transcription and production of pro-inflammatory interleukins (ILs), down-regulated expression of the skin barrier proteins filaggrin and loricrin, and upregulated phosphorylation of ERK, JNK and p38 in HaCaT cells. Inhibition of MAPK signaling rescued filaggrin expression in Der p 39-treated cells. Conclusions: The HDM allergen Der p 39 enhances allergic inflammation and promotes MAPK pathway-mediated epidermal barrier dysfunction, suggesting that Der p 39 may possess pathogenic and clinically relevant immunomodulatory potential. |
| format | Article |
| id | doaj-art-72e732e20936458c83f0bca7ecd1bc35 |
| institution | DOAJ |
| issn | 1939-4551 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | World Allergy Organization Journal |
| spelling | doaj-art-72e732e20936458c83f0bca7ecd1bc352025-08-20T02:50:45ZengElsevierWorld Allergy Organization Journal1939-45512025-03-0118310103610.1016/j.waojou.2025.101036The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunctionShan Liu, BSc0Ze-Lang Cai, MS1Jingcheng Liu2Si-Yi Que, BSc3Wan-Zhen Hu, MS4Liang Chen, MS5Jia-Jie Chen, PhD6Kunmei Ji, PhD7Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, Shenzhen 518055, ChinaDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, Shenzhen 518055, ChinaShenzhen College of International Education, Shenzhen 518048, ChinaDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, Shenzhen 518055, ChinaShenzhen University General Hospital, Shenzhen University, Shenzhen 518055, ChinaDepartment of Respiratory Medicine, Xiamen Changgung Hospital, Huaqiao University, Xiamen 361028, ChinaDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, Shenzhen 518055, China; Corresponding author. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, No. 1066 Xueyuan Road, Nanshan District, Shenzhen 518055, China.Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, Shenzhen 518055, China; Corresponding author. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen University, No. 1066 Xueyuan Road, Nanshan District, Shenzhen 518055, China.Background: House dust mite (HDM) allergens can induce or exacerbate allergic inflammation, including atopic dermatitis (AD). Substances that damage the epithelial barrier can trigger or worsen AD. The mechanism by which the novel HDM allergen Der p 39 induces allergic inflammation remains unclear. Our aim was to investigate the effects of Der p 39 on AD-like inflammation and associated mechanisms. Methods: Dinitrochlorobenzene (DNCB) and Der p 39 were utilized to establish AD model mice. Inflammation severity was evaluated with physiological and morphological assays. The effects of Der p 39 on inflammatory cytokine release and skin barrier protein expression were examined in HaCaT cells (human epidermal keratinocytes). Mitogen-activated protein kinase (MAPK) activation was examined by western blots. MAPK inhibitors were employed to assess MAPK involvement in filaggrin expression. Results: Der p 39 worsened allergic inflammation (tissue thickness) in murine ears pretreated with 1% DNCB. Compared to controls, Der p 39-sensitized tissues showed epidermal and dermal thickening with elevated numbers of mast cells and eosinophils in inflammatory lesions. Der p 39 increased transcription and production of pro-inflammatory interleukins (ILs), down-regulated expression of the skin barrier proteins filaggrin and loricrin, and upregulated phosphorylation of ERK, JNK and p38 in HaCaT cells. Inhibition of MAPK signaling rescued filaggrin expression in Der p 39-treated cells. Conclusions: The HDM allergen Der p 39 enhances allergic inflammation and promotes MAPK pathway-mediated epidermal barrier dysfunction, suggesting that Der p 39 may possess pathogenic and clinically relevant immunomodulatory potential.http://www.sciencedirect.com/science/article/pii/S1939455125000110House dust miteDer p 39Skin barrierAtopic dermatitisSkin inflammation |
| spellingShingle | Shan Liu, BSc Ze-Lang Cai, MS Jingcheng Liu Si-Yi Que, BSc Wan-Zhen Hu, MS Liang Chen, MS Jia-Jie Chen, PhD Kunmei Ji, PhD The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunction World Allergy Organization Journal House dust mite Der p 39 Skin barrier Atopic dermatitis Skin inflammation |
| title | The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunction |
| title_full | The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunction |
| title_fullStr | The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunction |
| title_full_unstemmed | The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunction |
| title_short | The novel house dust mite allergen Der p 39 exacerbates atopic dermatitis-like inflammation in mice by inducing skin barrier dysfunction |
| title_sort | novel house dust mite allergen der p 39 exacerbates atopic dermatitis like inflammation in mice by inducing skin barrier dysfunction |
| topic | House dust mite Der p 39 Skin barrier Atopic dermatitis Skin inflammation |
| url | http://www.sciencedirect.com/science/article/pii/S1939455125000110 |
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