IL-18基因敲除可减轻MC903在小鼠模型中诱发的特应性皮炎样皮肤损伤。,International Journal of Molecular Medicine

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IL-18基因敲除可减轻MC903在小鼠模型中诱发的特应性皮炎样皮肤损伤。
International Journal of Molecular Medicine ( IF 5.7 ) Pub Date : 2020-06-04 , DOI: 10.3892/ijmm.2020.4630
Jia-Long Chen ₁ , Xue-Li Niu ₁ , Ya-Li Gao ₁ , Lei Ma ₂ , Xing-Hua Gao ₁ , Hong-Duo Chen ₁ , Rui-Qun Qi ₁

Affiliation

白细胞介素（IL）-18，一种促炎性细胞因子，在多种皮肤疾病中起着重要作用。本研究的目的是研究IL-18在特应性皮炎（AD）发生中的作用。为此，将小鼠分为4组（n = 5 /组），如下：i）野生型（WT）对照；ii）IL18基因敲除（KO）对照; iii）MC903处理的野生型小鼠；iv）MC903治疗的KO小鼠。每天连续15天将MC903（乙醇中的4 nmol）局部应用到裸露的小鼠皮肤上。通过AD评分（SCORAD）评估AD样症状和严重程度。使用酶联免疫吸附测定法测定血清免疫球蛋白E（IgE）和胸腺基质淋巴细胞生成素（TSLP）的水平。免疫组织化学用于评估IL ‑1β的表达，皮肤病变中的信号转导和转录激活子（STAT）3和丝蛋白（FLG）。进行RT-qPCR评估皮肤病变中IL-1β，IL-4，IL-9，STAT3，促肾上腺皮质激素释放激素受体（CRHR）1，CRHR2，TSLP和caspase-1的mRNA水平。结果表明，IL-18可能在AD样病变的发展中起多效促炎性细胞因子的作用。IL-18 KO减轻了由MC903引起的加重的AD样病变，部分是通过上调Th2细胞因子来实现的。IL-18促进了表皮中FLG的表达和AD样病变中CRHR2的表达，但下调了IgE的血清水平。总体而言，本研究的发现表明，IL-18缺乏症减轻了AD诱发的小鼠病变。皮肤病变中的IL-9，STAT3，促肾上腺皮质激素释放激素受体（CRHR）1，CRHR2，TSLP和caspase-1。结果表明，IL-18可能在AD样病变的发展中起多效促炎性细胞因子的作用。IL-18 KO减轻了由MC903引起的加重的AD样病变，部分是通过上调Th2细胞因子来实现的。IL-18促进了表皮中FLG的表达和AD样病变中CRHR2的表达，但下调了IgE的血清水平。总体而言，本研究的发现表明，IL-18缺乏症减轻了AD诱发的小鼠病变。皮肤病变中的IL-9，STAT3，促肾上腺皮质激素释放激素受体（CRHR）1，CRHR2，TSLP和caspase-1。结果表明，IL-18可能在AD样病变的发展中起多效促炎性细胞因子的作用。IL-18 KO减轻了由MC903引起的加重的AD样病变，部分是通过上调Th2细胞因子来实现的。IL-18促进了表皮中FLG的表达和AD样病变中CRHR2的表达，但下调了IgE的血清水平。总体而言，本研究的发现表明，IL-18缺乏症减轻了AD诱发的小鼠病变。IL-18 KO减轻了由MC903引起的加重的AD样病变，部分是通过上调Th2细胞因子来实现的。IL-18促进了表皮中FLG的表达和AD样病变中CRHR2的表达，但下调了IgE的血清水平。总体而言，本研究的发现表明，IL-18缺乏症减轻了AD诱发的小鼠病变。IL-18 KO减轻了由MC903引起的加重的AD样病变，部分是通过上调Th2细胞因子。IL-18促进了FLG在表皮中的表达以及CR-2在AD样病变中的表达，但下调了IgE的血清水平。总体而言，本研究的发现表明，IL-18缺乏症减轻了AD诱发的小鼠病变。

"点击查看英文标题和摘要"

IL‑18 knockout alleviates atopic dermatitis‑like skin lesions induced by MC903 in a mouse model.

Interleukin (IL)‑18, a pro‑inflammatory cytokine, plays an important role in a number of skin diseases. The aim of the present study was to investigate the role of IL‑18 in the development of atopic dermatitis (AD). For this purpose, mice were divided into 4 groups (n=5/group) as follows: i) The wild‑type (WT) controls; ii) IL18 knockout (KO) controls; iii) MC903‑treated WT mice; and iv) MC903‑treated KO mice. MC903 (4 nmol in ethanol) was topically applied daily for 15 consecutive days to the exposed skins of mice. AD‑like symptoms and severity were evaluated by the scoring of AD (SCORAD). Serum immunoglobulin E (IgE) and thymic stromal lymphopoietin (TSLP) levels were determined with the use of an enzyme‑linked immunosorbent assay. Immunohistochemistry was used to assess the expression of IL‑1β, signal transducer and activator of transcription (STAT)3 and filaggrin (FLG) in the skin lesions. RT‑qPCR was performed to assess the mRNA levels of IL‑1β, IL‑4, IL‑9, STAT3, corticotropin‑releasing hormone receptor (CRHR)1, CRHR2, TSLP and caspase‑1 in the skin lesions. It was demonstrated that IL‑18 may function as a pleiotropic pro‑inflammatory cytokine in the development of AD‑like lesions. IL‑18 KO reduced aggravated AD‑like lesions induced by MC903, in part by upregulating Th2 cytokines. IL‑18 promoted the expression of FLG in the epidermis and CRHR2 in AD‑like lesions, but downregulated the serum levels of IgE. On the whole, the findings of the present study demonstrate that IL‑18 deficiency alleviates AD‑induced lesions in mice.

更新日期：2020-08-21

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