Staphylococcus aureus SOS response: Activation, impact, and drug targets.

IF 4.5 Q1 MICROBIOLOGY
mLife Pub Date : 2024-09-30 eCollection Date: 2024-09-01 DOI:10.1002/mlf2.12137
Kaiying Cheng, Yukang Sun, Huan Yu, Yingxuan Hu, Yini He, Yuanyuan Shen
{"title":"<i>Staphylococcus aureus</i> SOS response: Activation, impact, and drug targets.","authors":"Kaiying Cheng, Yukang Sun, Huan Yu, Yingxuan Hu, Yini He, Yuanyuan Shen","doi":"10.1002/mlf2.12137","DOIUrl":null,"url":null,"abstract":"<p><p><i>Staphylococcus aureus</i> is a common cause of diverse infections, ranging from superficial to invasive, affecting both humans and animals. The widespread use of antibiotics in clinical treatments has led to the emergence of antibiotic-resistant strains and small colony variants. This surge presents a significant challenge in eliminating infections and undermines the efficacy of available treatments. The bacterial Save Our Souls (SOS) response, triggered by genotoxic stressors, encompasses host immune defenses and antibiotics, playing a crucial role in bacterial survival, invasiveness, virulence, and drug resistance. Accumulating evidence underscores the pivotal role of the SOS response system in the pathogenicity of <i>S. aureus</i>. Inhibiting this system offers a promising approach for effective bactericidal treatments and curbing the evolution of antimicrobial resistance. Here, we provide a comprehensive review of the activation, impact, and key proteins associated with the SOS response in <i>S. aureus</i>. Additionally, perspectives on therapeutic strategies targeting the SOS response for <i>S. aureus</i>, both individually and in combination with traditional antibiotics are proposed.</p>","PeriodicalId":94145,"journal":{"name":"mLife","volume":"3 3","pages":"343-366"},"PeriodicalIF":4.5000,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442139/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"mLife","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/mlf2.12137","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Staphylococcus aureus is a common cause of diverse infections, ranging from superficial to invasive, affecting both humans and animals. The widespread use of antibiotics in clinical treatments has led to the emergence of antibiotic-resistant strains and small colony variants. This surge presents a significant challenge in eliminating infections and undermines the efficacy of available treatments. The bacterial Save Our Souls (SOS) response, triggered by genotoxic stressors, encompasses host immune defenses and antibiotics, playing a crucial role in bacterial survival, invasiveness, virulence, and drug resistance. Accumulating evidence underscores the pivotal role of the SOS response system in the pathogenicity of S. aureus. Inhibiting this system offers a promising approach for effective bactericidal treatments and curbing the evolution of antimicrobial resistance. Here, we provide a comprehensive review of the activation, impact, and key proteins associated with the SOS response in S. aureus. Additionally, perspectives on therapeutic strategies targeting the SOS response for S. aureus, both individually and in combination with traditional antibiotics are proposed.

金黄色葡萄球菌的 SOS 反应:激活、影响和药物靶点。
金黄色葡萄球菌是引起各种感染的常见原因,从浅表性感染到侵入性感染,对人类和动物都有影响。抗生素在临床治疗中的广泛使用导致耐抗生素菌株和小菌落变种的出现。这种激增给消除感染带来了巨大挑战,并削弱了现有疗法的疗效。细菌的 "拯救灵魂"(SOS)反应是由基因毒性应激源引发的,包括宿主免疫防御系统和抗生素,在细菌的生存、侵袭性、毒性和耐药性方面起着至关重要的作用。越来越多的证据强调了 SOS 反应系统在金黄色葡萄球菌致病性中的关键作用。抑制该系统为有效的杀菌治疗和遏制抗菌药耐药性的进化提供了一种可行的方法。在此,我们对金黄色葡萄球菌 SOS 反应的激活、影响和相关关键蛋白进行了全面综述。此外,我们还提出了针对金黄色葡萄球菌 SOS 反应的治疗策略,包括单独使用和与传统抗生素联合使用。
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 求助全文
来源期刊
CiteScore
2.30
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信