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IL-32 通过激活 JAK1/miR-155 轴促进特应性皮炎的发生。

IL-32 promotes the occurrence of atopic dermatitis by activating the JAK1/microRNA-155 axis.

机构信息

Department of Dermatology, Hunan Children's Hospital, No. 68 Ziyuan Road, Changsha, 410007, People's Republic of China.

出版信息

J Transl Med. 2022 May 11;20(1):207. doi: 10.1186/s12967-022-03375-x.

DOI:10.1186/s12967-022-03375-x
PMID:35545774
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9097387/
Abstract

BACKGROUND

This study aims to explore the mechanism of interleukin-32 (IL-32) affecting atopic dermatitis (AD) through the Janus-activated kinase-1 (JAK1)/microRNA-155 (miR-155) axis.

METHODS

In this study, skin tissue samples and blood samples from normal subjects and patients with AD, human immortalized keratinocytes (HaCaT), and PA-induced mouse models of AD were selected for expression determination of IL-32, JAK1 and miR-155. The interaction among IL-32, JAK1 and miR-155 was identified with their roles in AD analyzed through loss- and gain-of-function assays.

RESULTS

Elevated IL-32 was detected in AD tissues and blood samples and promoted the occurrence of AD. IL-32 upregulated JAK1 expression and phosphorylation of its downstream genes, thus activating the JAK signaling pathway. JAK1 promoted the expression of miR-155. IL-32/JAK1/miR-155 axis promoted inflammation in the AD skin reconstruction model. In vivo experiments further confirmed that IL-32 promoted AD development by activating the JAK1/miR-155 axis.

CONCLUSION

The present study underlined that IL-32 promoted the occurrence of AD by promoting JAK1 expression to upregulate miR-155 expression.

摘要

背景

本研究旨在通过 Janus 激活激酶 1（JAK1）/微小 RNA-155（miR-155）轴探讨白细胞介素 32（IL-32）影响特应性皮炎（AD）的机制。

方法

本研究选取正常受试者和 AD 患者的皮肤组织样本和血液样本、人永生化角质形成细胞（HaCaT）和 PA 诱导的 AD 小鼠模型，检测 IL-32、JAK1 和 miR-155 的表达。通过缺失和功能获得实验分析 IL-32、JAK1 和 miR-155 之间的相互作用及其在 AD 中的作用。

结果

AD 组织和血液样本中检测到 IL-32 升高，促进 AD 的发生。IL-32 上调 JAK1 表达及其下游基因的磷酸化，从而激活 JAK 信号通路。JAK1 促进 miR-155 的表达。IL-32/JAK1/miR-155 轴促进 AD 皮肤重建模型中的炎症。体内实验进一步证实，IL-32 通过激活 JAK1/miR-155 轴促进 AD 发展。

结论

本研究强调，IL-32 通过促进 JAK1 表达来上调 miR-155 表达，从而促进 AD 的发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/66e4fd963418/12967_2022_3375_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/f74ba2c529ae/12967_2022_3375_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/574792e260ee/12967_2022_3375_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/ba3c00ed8a7b/12967_2022_3375_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/57049fd5dc82/12967_2022_3375_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/8d44496e75a9/12967_2022_3375_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/6a84c5326f77/12967_2022_3375_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/66e4fd963418/12967_2022_3375_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/f74ba2c529ae/12967_2022_3375_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/574792e260ee/12967_2022_3375_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/ba3c00ed8a7b/12967_2022_3375_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/57049fd5dc82/12967_2022_3375_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/8d44496e75a9/12967_2022_3375_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/6a84c5326f77/12967_2022_3375_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7ca/9097387/66e4fd963418/12967_2022_3375_Fig7_HTML.jpg

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