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卡泊三醇对培养的人角质形成细胞中人类β-防御素-2和LL-37表达的影响。

The effect of calcipotriol on the expression of human beta defensin-2 and LL-37 in cultured human keratinocytes.

作者信息

Kim Beom Joon, Rho Yong Kwan, Lee Hye In, Jeong Mi Sook, Li Kapsok, Seo Seong Jun, Kim Myeung Nam, Hong Chang Kwun

机构信息

Department of Dermatology, Chung-Ang Medical Research Center, College of Medicine, Chung-Ang University, Seoul 156-755, South Korea.

出版信息

Clin Dev Immunol. 2009;2009:645898. doi: 10.1155/2009/645898. Epub 2010 Feb 22.

DOI:10.1155/2009/645898
PMID:20182640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2825796/
Abstract

BACKGROUND

Vitamin D has been reported to regulate innate immunity by controlling the expression of antimicrobial peptides (AMPs).

OBJECTIVE

We investigated the effect of calcipotriol on the expression of AMPs in human cultured keratinocytes.

METHODS

Keratinocytes were treated with lipopolysaccharide (LPS), TNF-alpha, Calcipotriol and irradiated with UVB, cultured, and harvested. To assess the expression of human beta defensin-2 and LL-37 in the control group, not exposed to any stimulants, the experimental group was treated with LPS, TNF-alpha, or UVB, and another group was treated again with calcipotriol; reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemical staining were performed.

RESULTS

In the experimental group treated with LPS, UVB irradiation, and TNF-alpha, the expression of beta-defensin and LL-37 was increased more than in the control group and then decreased in the experimental group treated with calcipotriol.

CONCLUSIONS

Calcipotriol suppressed HBD-2 and LL-37, which were stimulated by UVB, LPS, and TNF-alpha.

摘要

背景

据报道，维生素D通过控制抗菌肽（AMPs）的表达来调节固有免疫。

目的

我们研究了卡泊三醇对人培养角质形成细胞中AMPs表达的影响。

方法

用脂多糖（LPS）、肿瘤坏死因子-α（TNF-α）、卡泊三醇处理角质形成细胞，并进行紫外线B（UVB）照射，然后培养并收获细胞。为评估未暴露于任何刺激物的对照组中人β-防御素-2和LL-37的表达，实验组分别用LPS、TNF-α或UVB处理，另一组再用卡泊三醇处理；进行逆转录-聚合酶链反应、蛋白质印迹法和免疫组织化学染色。

结果

在用LPS、UVB照射和TNF-α处理的实验组中，β-防御素和LL-37的表达比对照组增加得更多，然后在用卡泊三醇处理的实验组中下降。

结论

卡泊三醇抑制了由UVB、LPS和TNF-α刺激产生的HBD-2和LL-37。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5b3/2825796/57d5b532b589/CDI2009-645898.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5b3/2825796/017d594688ce/CDI2009-645898.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5b3/2825796/4f1e6962b432/CDI2009-645898.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5b3/2825796/57d5b532b589/CDI2009-645898.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5b3/2825796/017d594688ce/CDI2009-645898.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5b3/2825796/4f1e6962b432/CDI2009-645898.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5b3/2825796/57d5b532b589/CDI2009-645898.003.jpg

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