Staphylococcus aureus Proteases: Orchestrators of Skin Inflammation.

DNA and cell biology Pub Date : 2024-10-01 Epub Date: 2024-07-03 DOI:10.1089/dna.2024.0134
Sabrina N Kline, Yoshine Saito, Nathan K Archer
{"title":"<i>Staphylococcus aureus</i> Proteases: Orchestrators of Skin Inflammation.","authors":"Sabrina N Kline, Yoshine Saito, Nathan K Archer","doi":"10.1089/dna.2024.0134","DOIUrl":null,"url":null,"abstract":"<p><p>Skin homeostasis relies on a delicate balance between host proteases and protease inhibitors along with those secreted from microbial communities, as disruption to this harmony contributes to the pathogenesis of inflammatory skin disorders, including atopic dermatitis and Netherton's syndrome. In addition to being a prominent cause of skin and soft tissue infections, the gram-positive bacterium <i>Staphylococcus aureus</i> is a key player in inflammatory skin conditions due to its array of 10 secreted proteases. Herein we review how <i>S. aureus</i> proteases augment the development of inflammation in skin disorders. These mechanisms include degradation of skin barrier integrity, immune dysregulation and pruritis, and impairment of host defenses. Delineating the diverse roles of <i>S. aureus</i> proteases has the potential to reveal novel therapeutic strategies, such as inhibitors of proteases or their cognate target, as well as neutralizing vaccines to alleviate the burden of inflammatory skin disorders in patients.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"483-491"},"PeriodicalIF":0.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11535466/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"DNA and cell biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/dna.2024.0134","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/3 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Skin homeostasis relies on a delicate balance between host proteases and protease inhibitors along with those secreted from microbial communities, as disruption to this harmony contributes to the pathogenesis of inflammatory skin disorders, including atopic dermatitis and Netherton's syndrome. In addition to being a prominent cause of skin and soft tissue infections, the gram-positive bacterium Staphylococcus aureus is a key player in inflammatory skin conditions due to its array of 10 secreted proteases. Herein we review how S. aureus proteases augment the development of inflammation in skin disorders. These mechanisms include degradation of skin barrier integrity, immune dysregulation and pruritis, and impairment of host defenses. Delineating the diverse roles of S. aureus proteases has the potential to reveal novel therapeutic strategies, such as inhibitors of proteases or their cognate target, as well as neutralizing vaccines to alleviate the burden of inflammatory skin disorders in patients.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
金黄色葡萄球菌蛋白酶:皮肤炎症的协调者。
皮肤的平衡有赖于宿主蛋白酶和蛋白酶抑制剂以及微生物群落分泌的蛋白酶抑制剂之间的微妙平衡,破坏这种和谐会导致炎症性皮肤病的发病,包括特应性皮炎和奈瑟顿综合征。除了是皮肤和软组织感染的主要病因外,革兰氏阳性菌金黄色葡萄球菌还因其分泌的 10 种蛋白酶而在皮肤炎症中扮演重要角色。在此,我们回顾了金黄色葡萄球菌蛋白酶是如何促进皮肤疾病炎症发展的。这些机制包括皮肤屏障完整性退化、免疫调节失调和瘙痒症以及宿主防御功能受损。阐明金黄色葡萄球菌蛋白酶的不同作用有可能揭示新的治疗策略,如蛋白酶抑制剂或其同源靶点,以及中和疫苗,以减轻炎症性皮肤病患者的负担。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
VIRMA-Mediated the m6A Methylation of SCD Facilitates Wilms' Tumor Progression via AMPK Pathway. Liquiritin as a Tumor Suppressor Prevents the Development of Breast Cancer via the Epidermal Growth Factor Receptor/Mitogen-Activated Protein Kinase 8 Signaling Pathway. The Role of microRNAs in Lidocaine-Induced Spinal Cord Neurotoxicity: An Exploration Based on Bioinformatics Analysis. Identification and Analysis of Autophagy-Related Genes as Diagnostic Markers and Potential Therapeutic Targets for Tuberculosis Through Bioinformatics. METTL3-Induced m6A Modification Enhances Hsa_Circ_0136959 Expression to Impair the Tumor Characteristics of Papillary Thyroid Carcinoma via Accelerating Ferroptosis.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1