The Role of Lipopolysaccharide-Induced Cell Signalling in Chronic Inflammation.

Q1 Psychology
Chronic Stress Pub Date : 2022-02-08 eCollection Date: 2022-01-01 DOI:10.1177/24705470221076390
Martin J Page, Douglas B Kell, Etheresia Pretorius
{"title":"The Role of Lipopolysaccharide-Induced Cell Signalling in Chronic Inflammation.","authors":"Martin J Page,&nbsp;Douglas B Kell,&nbsp;Etheresia Pretorius","doi":"10.1177/24705470221076390","DOIUrl":null,"url":null,"abstract":"<p><p>Lipopolysaccharide (LPS) is the main structural component of the outer membrane of most Gram-negative bacteria and has diverse immunostimulatory and procoagulant effects. Even though LPS is well described for its role in the pathology of sepsis, considerable evidence demonstrates that LPS-induced signalling and immune dysregulation are also relevant in the pathophysiology of many diseases, characteristically where endotoxaemia is less severe. These diseases are typically chronic and progressive in nature and span broad classifications, including neurodegenerative, metabolic, and cardiovascular diseases. This Review reappraises the mechanisms of LPS-induced signalling and emphasises the crucial contribution of LPS to the pathology of multiple chronic diseases, beyond conventional sepsis. This perspective asserts that new ways of approaching chronic diseases by targeting LPS-driven pathways may be of therapeutic benefit in a wide range of chronic inflammatory conditions.</p>","PeriodicalId":52315,"journal":{"name":"Chronic Stress","volume":" ","pages":"24705470221076390"},"PeriodicalIF":0.0000,"publicationDate":"2022-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8e/d4/10.1177_24705470221076390.PMC8829728.pdf","citationCount":"56","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chronic Stress","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/24705470221076390","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"Psychology","Score":null,"Total":0}
引用次数: 56

Abstract

Lipopolysaccharide (LPS) is the main structural component of the outer membrane of most Gram-negative bacteria and has diverse immunostimulatory and procoagulant effects. Even though LPS is well described for its role in the pathology of sepsis, considerable evidence demonstrates that LPS-induced signalling and immune dysregulation are also relevant in the pathophysiology of many diseases, characteristically where endotoxaemia is less severe. These diseases are typically chronic and progressive in nature and span broad classifications, including neurodegenerative, metabolic, and cardiovascular diseases. This Review reappraises the mechanisms of LPS-induced signalling and emphasises the crucial contribution of LPS to the pathology of multiple chronic diseases, beyond conventional sepsis. This perspective asserts that new ways of approaching chronic diseases by targeting LPS-driven pathways may be of therapeutic benefit in a wide range of chronic inflammatory conditions.

Abstract Image

Abstract Image

Abstract Image

脂多糖诱导的细胞信号传导在慢性炎症中的作用。
脂多糖(LPS)是大多数革兰氏阴性菌外膜的主要结构成分,具有多种免疫刺激和促凝作用。尽管LPS在脓毒症病理中的作用已被很好地描述,但大量证据表明,LPS诱导的信号传导和免疫失调也与许多疾病的病理生理有关,尤其是内毒素血症不太严重的疾病。这些疾病通常是慢性和进行性的,分类广泛,包括神经退行性、代谢性和心血管疾病。本综述重新评估了脂多糖诱导的信号传导机制,并强调了脂多糖对多种慢性疾病病理的重要贡献,而不仅仅是传统的败血症。这一观点认为,通过靶向lps驱动途径治疗慢性疾病的新方法可能对多种慢性炎症有治疗益处。
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
Chronic Stress
Chronic Stress Psychology-Clinical Psychology
CiteScore
7.40
自引率
0.00%
发文量
25
审稿时长
6 weeks
×
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:604180095
Book学术官方微信