Wu Xia, Zhao Yan, Gu Ying, Li Kun, Wang Xiaojie, Zhang Jianzhong
Department of Dermatology, Peking University People's Hospital, Beijing, China.
Department of Dermatology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Front Pharmacol. 2021 Mar 22;12:652302. doi: 10.3389/fphar.2021.652302. eCollection 2021.
Atopic dermatitis (AD) is a common inflammatory skin disease. () colonization in skin lesions occurs in approximately 70% of AD patients. It has been found that IFN-λ1 can inhibit the colonization of in normal human nasal mucosa. IFN-λ1 can increase IL-28RA in infected human keratinocytes. In this study, we found that IFN-λ1 can increase mRNA expression of FLG and antimicrobial peptides (AMPs) and inhibit TSLP mRNA expression in infected human keratinocytes. IFN-λ1 can increase intracellular ROS level, decrease STAT1 phosphorylation, and inhibit the colonization of in human primary keratinocytes. These effects were attenuated by knocking-down IL-28R and NADPH oxidase inhibitor, suggesting that this function was mediated by JAK-STAT1 signaling pathway. These results suggest that IFN-λ1 might have an inhibitory effect on colonization in AD lesions. Our findings might have potential value in the treatment for AD.
特应性皮炎(AD)是一种常见的炎症性皮肤病。约70%的AD患者皮肤损伤处会发生()定植。研究发现,IFN-λ1可抑制其在正常人鼻黏膜中的定植。IFN-λ1可增加受感染的人角质形成细胞中IL-28RA的表达。在本研究中,我们发现IFN-λ1可增加受感染的人角质形成细胞中FLG和抗菌肽(AMPs)的mRNA表达,并抑制TSLP mRNA表达。IFN-λ1可增加细胞内ROS水平,降低STAT1磷酸化,并抑制其在人原代角质形成细胞中的定植。敲低IL-28R和NADPH氧化酶抑制剂可减弱这些作用,表明该功能是由JAK-STAT1信号通路介导的。这些结果表明,IFN-λ1可能对AD皮损中的()定植具有抑制作用。我们的发现可能对AD的治疗具有潜在价值。