霉菌感染过程中线粒体活性氧的宿主和微生物调控。

IF 3.9 3区 生物学 Q2 CELL BIOLOGY
Jin Kyung Kim , Eun-Kyeong Jo
{"title":"霉菌感染过程中线粒体活性氧的宿主和微生物调控。","authors":"Jin Kyung Kim ,&nbsp;Eun-Kyeong Jo","doi":"10.1016/j.mito.2024.101852","DOIUrl":null,"url":null,"abstract":"<div><p>Mycobacteria, including <em>Mycobacterium tuberculosis</em> (Mtb) and non-tuberculous mycobacteria (NTM), pose challenges in treatment due to their increased resistance to antibiotics. Following infection, mycobacteria and their components trigger robust innate and inflammatory immune responses intricately associated with the modulation of mitochondrial functions, including oxidative phosphorylation (OXPHOS) and metabolism. Certainly, mitochondrial reactive oxygen species (mtROS) are an inevitable by-product of OXPHOS and function as a bactericidal weapon; however, an excessive accumulation of mtROS are linked to pathological inflammation and necroptotic cell death during mycobacterial infection. Despite previous studies outlining various host pathways involved in regulating mtROS levels during antimicrobial responses in mycobacterial infection, our understanding of the precise mechanisms orchestrating the fine regulation of this response remains limited. Emerging evidence suggests that mycobacterial proteins play a role in targeting the mitochondria of the host, indicating the potential influence of microbial factors on mitochondrial functions within host cells. In this review, we provide an overview of how both host and Mtb factors influence mtROS generation during infection. A comprehensive study of host and microbial factors that target mtROS will shed light on innovative approaches for effectively managing drug-resistant mycobacterial infections.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"75 ","pages":"Article 101852"},"PeriodicalIF":3.9000,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Host and microbial regulation of mitochondrial reactive oxygen species during mycobacterial infections\",\"authors\":\"Jin Kyung Kim ,&nbsp;Eun-Kyeong Jo\",\"doi\":\"10.1016/j.mito.2024.101852\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Mycobacteria, including <em>Mycobacterium tuberculosis</em> (Mtb) and non-tuberculous mycobacteria (NTM), pose challenges in treatment due to their increased resistance to antibiotics. Following infection, mycobacteria and their components trigger robust innate and inflammatory immune responses intricately associated with the modulation of mitochondrial functions, including oxidative phosphorylation (OXPHOS) and metabolism. Certainly, mitochondrial reactive oxygen species (mtROS) are an inevitable by-product of OXPHOS and function as a bactericidal weapon; however, an excessive accumulation of mtROS are linked to pathological inflammation and necroptotic cell death during mycobacterial infection. Despite previous studies outlining various host pathways involved in regulating mtROS levels during antimicrobial responses in mycobacterial infection, our understanding of the precise mechanisms orchestrating the fine regulation of this response remains limited. Emerging evidence suggests that mycobacterial proteins play a role in targeting the mitochondria of the host, indicating the potential influence of microbial factors on mitochondrial functions within host cells. In this review, we provide an overview of how both host and Mtb factors influence mtROS generation during infection. A comprehensive study of host and microbial factors that target mtROS will shed light on innovative approaches for effectively managing drug-resistant mycobacterial infections.</p></div>\",\"PeriodicalId\":18606,\"journal\":{\"name\":\"Mitochondrion\",\"volume\":\"75 \",\"pages\":\"Article 101852\"},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2024-02-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Mitochondrion\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1567724924000102\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mitochondrion","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1567724924000102","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

分枝杆菌,包括结核分枝杆菌(Mtb)和非结核分枝杆菌(NTM),由于对抗生素的耐药性增强,给治疗带来了挑战。感染分枝杆菌后,分枝杆菌及其成分会引发强烈的先天性免疫反应和炎症反应,这些反应与线粒体功能(包括氧化磷酸化(OXPHOS)和新陈代谢)的调节密切相关。当然,线粒体活性氧(mtROS)是氧化磷酸化过程中不可避免的副产品,也是一种杀菌武器;然而,在分枝杆菌感染期间,线粒体活性氧的过度积累与病理性炎症和坏死细胞的死亡有关。尽管以前的研究概述了在分枝杆菌感染的抗菌反应过程中参与调节 mtROS 水平的各种宿主途径,但我们对这种反应的精确调节机制的了解仍然有限。新的证据表明,分枝杆菌蛋白在以宿主线粒体为靶标方面发挥了作用,这表明微生物因子对宿主细胞内的线粒体功能具有潜在影响。在本综述中,我们将概述宿主和Mtb因子如何在感染过程中影响线粒体ROS的产生。对针对 mtROS 的宿主和微生物因素的全面研究将为有效控制耐药分枝杆菌感染的创新方法提供启示。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Host and microbial regulation of mitochondrial reactive oxygen species during mycobacterial infections

Host and microbial regulation of mitochondrial reactive oxygen species during mycobacterial infections

Mycobacteria, including Mycobacterium tuberculosis (Mtb) and non-tuberculous mycobacteria (NTM), pose challenges in treatment due to their increased resistance to antibiotics. Following infection, mycobacteria and their components trigger robust innate and inflammatory immune responses intricately associated with the modulation of mitochondrial functions, including oxidative phosphorylation (OXPHOS) and metabolism. Certainly, mitochondrial reactive oxygen species (mtROS) are an inevitable by-product of OXPHOS and function as a bactericidal weapon; however, an excessive accumulation of mtROS are linked to pathological inflammation and necroptotic cell death during mycobacterial infection. Despite previous studies outlining various host pathways involved in regulating mtROS levels during antimicrobial responses in mycobacterial infection, our understanding of the precise mechanisms orchestrating the fine regulation of this response remains limited. Emerging evidence suggests that mycobacterial proteins play a role in targeting the mitochondria of the host, indicating the potential influence of microbial factors on mitochondrial functions within host cells. In this review, we provide an overview of how both host and Mtb factors influence mtROS generation during infection. A comprehensive study of host and microbial factors that target mtROS will shed light on innovative approaches for effectively managing drug-resistant mycobacterial infections.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
×
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