Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis.

Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis.
复制标题

DOI:
10.1016/j.alit.2014.06.001
复制
发表时间:
2015-01
期刊:
Allergology international : official journal of the Japanese Society of Allergology
影响因子:
--
通讯作者:
Izuhara K
Izuhara K
中科院分区:
其他
文献类型:
--
作者:
Arima K;Ohta S;Takagi A;Shiraishi H;Masuoka M;Ontsuka K;Suto H;Suzuki S;Yamamoto K;Ogawa M;Simmons O;Yamaguchi Y;Toda S;Aihara M;Conway SJ;Ikeda S;Izuhara K

文献摘要

被引文献

相似文献

表皮增生是在特应性皮炎(AD)和银屑病中观察到的组织学标志,尽管这些疾病的临床特征和潜在的免疫学病症不同。我们以前表明,骨膜蛋白,一种基质细胞蛋白,在AD的表皮增生中起着至关重要的作用,使用小鼠模型和三维器官型共培养系统。在这项研究中,我们探讨了骨膜蛋白参与银屑病表皮增生的假设。为了检测骨膜蛋白在银屑病患者中的表达,我们对6例银屑病患者的皮肤活检组织进行了免疫组化分析。为了研究骨膜蛋白在银屑病发病机制中的作用,我们在用咪喹莫特(IMQ)局部治疗诱导的银屑病小鼠模型中评估了骨膜蛋白缺陷小鼠。骨膜蛋白在所有研究的银屑病患者的真皮中基本上表达。在骨膜蛋白缺乏小鼠中,IMQ治疗诱导的表皮增生受损,沿着皮肤肿胀减少。然而,在用IMQ治疗后,骨膜蛋白缺乏并不改变炎性细胞如中性粒细胞的浸润; IL-17、IL-22或IL-23的产生;或产生IL-17和IL-22的第3组先天淋巴细胞的诱导/扩增。骨膜蛋白在顶Q诱导的皮肤炎症中的表皮增生期间起重要作用,独立于IL-23-IL-17/IL-22轴。骨膜蛋白似乎是AD和银屑病常见的表皮增生的介质。
Epidermal hyperplasia is a histological hallmark observed in both atopic dermatitis (AD) and psoriasis, although the clinical features and the underlying immunological disorders of these diseases are different. We previously showed that periostin, a matricellular protein, plays a critical role in epidermal hyperplasia in AD, using a mouse model and a 3-dimensional organotypic coculture system. In this study, we explore the hypothesis that periostin is involved in epidermal hyperplasia in psoriasis. To examine expression of periostin in psoriasis patients, we performed immunohistochemical analysis on skin biopsies from six such patients. To investigate periostin’s role in the pathogenesis of psoriasis, we evaluated periostin-deficient mice in a psoriasis mouse model induced by topical treatment with imiquimod (IMQ). Periostin was substantially expressed in the dermis of all investigated psoriasis patients. Epidermal hyperplasia induced by IMQ treatment was impaired in periostin-deficient mice, along with decreased skin swelling. However, upon treatment with IMQ, periostin deficiency did not alter infiltration of inflammatory cells such as neutrophils; production of IL-17, –22, or –23; or induction/expansion of IL-17– and IL-22–producing group 3 innate lymphoid cells. Periostin plays an important role during epidermal hyperplasia in IMQ-induced skin inflammation, independently of the IL-23–IL-17/IL-22 axis. Periostin appears to be a mediator for epidermal hyperplasia that is common to AD and psoriasis.