Establishment of a mouse model for post‐inflammatory hyperpigmentation

Establishment of a mouse model for post‐inflammatory hyperpigmentation
复制标题

炎症后色素沉着过度小鼠模型的建立

DOI:
10.1111/pcmr.12911
复制
发表时间:
2020
影响因子:
4.3
通讯作者:
Suzuki Tamio
Suzuki Tamio
中科院分区:
医学3区
文献类型:
--
作者:
Nakano Shoko;Abe Yuko;Nakajima Kimiko;Sano Shigetoshi;Yamamoto Osamu;Wakamatsu Kazumasa;Ito Shosuke;Hayashi Masahiro;Suzuki Tamio

文献摘要

相似文献

炎症后色素沉着过度(PIH)是一种常见的皮肤病,可导致外观受损。然而,妊高征的病理生理学仍然知之甚少,至少在一定程度上,因为一个合适的动物模型的研究还没有建立。为了分析妊高征的病理机制,我们通过重复应用2,4-二硝基氟苯的半抗原,成功地在具有含有黑色素的人型表皮的无毛转基因小鼠(hk 14-SCF Tg/HRM)中诱导了妊高征。组织学观察显示,在引发特应性皮炎样病症后,真皮中出现表皮增生、主要炎症细胞浸润和含黑色素细胞。在第2周,这些发现与妊高征的特征相似,即表皮中黑色素增加而无海绵状增生或液体变性,真皮中噬黑素细胞增加。黑色素的动态分析表明,真皮中的黑色素比表皮中的黑色素保留更长的时间。此外,免疫组织化学染色显示,大多数含有黑色素的细胞对抗CD 68抗体呈阳性,但对抗F4/80抗体呈阴性。这些数据表明,新的治疗妊高征应针对巨噬细胞,并最终导致新的治疗方式的发展。
Post‐inflammatory hyperpigmentation (PIH) is a common cutaneous condition that can cause a disfigured appearance. However, the pathophysiology of PIH remains poorly understood, at least in part, because an appropriate animal model for research has not been established. In order to analyze the pathomechanism of PIH, we successfully induced PIH in a hairless version of transgenic mice (hk14‐SCF Tg/HRM) that have a human‐type epidermis containing melanin by repeated hapten application of 2,4‐dinitrofluorobenzene. Histopathologic observation showed epidermal hyperplasia, predominant infiltrations of inflammatory cells, and melanin‐containing cells in the dermis just after elicitation of the atopic dermatitis‐like condition. At week 2, the findings were similar to the characteristics of PIH, that is, an increase of melanin without spongiosis or liquid degeneration in the epidermis and an increase in dermal melanophages. Dynamic analysis of melanin showed that the melanin in the dermis remained for a longer duration than in the epidermis. Furthermore, immunohistochemical staining revealed that the majority of cells containing melanin were positive for the anti‐CD68 antibody, but negative for the anti‐F4/80 antibody. These data suggest that novel treatments of PIH should be targeted against macrophages and should eventually lead to the development of new treatment modalities.