title: Influence of different types of contact hypersensitivity on imiquimod-induced psoriasis-like inflammation in mice.
abstract: It is currently believed that psoriasis and allergic contact dermatitis (ACD) are different diseases; however, they share clinical similarities. The involvement of T helper 17 (Th17) cells in these disorders provides a novel opportunity to investigate the relationship between them. The present study aimed to determine whether the same or overlapping inflammatory pathways are involved in the two diseases, and the influence of different types of ACD on psoriasis. Compound mouse models of Th1 or Th2‑type contact hypersensitivity (CHS) combined with imiquimod (IMQ)‑induced psoriasis‑like inflammation were established, in order to mimic the characteristics of ACD and psoriasis. Histopathology, immunohistochemistry and cytokine detection in blood serum and tissues were used to compare the differences between the mice treated with IMQ alone or IMQ combined with Th1 and Th2‑type CHS. As compared with the IMQ‑treated mice or IMQ-treated Th1‑type CHS mice, the mice with Th2‑type CHS treated with IMQ exhibited more serious psoriasis‑like inflammation with increased epidermal thickness and infiltrating cells in the derma. High mRNA expression levels of interleukin (IL)‑17, IL‑22, IL‑23, TNF‑α and RORγt were detected in back skin lesions. Additionally, high levels of IL‑17 and IL‑22 in blood serum were detected in IMQ‑treated mice combined with Th2‑type CHS. The mice treated with IMQ alone, and IMQ treatment combined with Th1‑type CHS had a comparable psoriasis‑like inflammatory response in the back skin. In conclusion, these data demonstrate that Th2‑type CHS exacerbated the IMQ‑treated psoriatic inflammation of mice via the IL‑23/IL‑17 axis. Th17 cells and associated pathways may link ACD and psoriasis. Therefore, patients with psoriasis should avoid contact with specific sensitizers, such as fragrance and rubber products, which may induce Th2 polarization.
authors.affiliation: Department of Dermatology and Venereology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Bai
authors.affiliation: Department of Dermatology and Venereology, The University of Hong Kong‑Shenzhen Hospital, Shenzhen, Guangdong 518053, P.R. China.
authors.forename: Zhenying
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Department of Dermatology and Venereology, The University of Hong Kong‑Shenzhen Hospital, Shenzhen, Guangdong 518053, P.R. China.
authors.forename: Suchun
authors.initials: S
authors.lastname: Hou
authors.affiliation: Department of Dermatology and Venereology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China.
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Liu
mesh_terms: D000634:Aminoquinolines / Q000009:adverse effects*; D000818:Animals; D015415:Biomarkers; D016207:Cytokines / Q000097:blood / Q000235:genetics / Q000378:metabolism; D003877:Dermatitis, Contact / Q000150:complications* / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D000077271:Imiquimod; D051379:Mice; D011565:Psoriasis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D012867:Skin / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
chemical_list: D000634:Aminoquinolines; D015415:Biomarkers; D016207:Cytokines; D000077271:Imiquimod