先天免疫激活引起的中枢神经系统细胞损伤:从胞内细菌流产布鲁氏菌中吸取的教训。

IF 2.4 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Ana María Rodríguez, Julia Rodríguez, Alex D Guano, Guillermo H Giambartolomei
{"title":"先天免疫激活引起的中枢神经系统细胞损伤:从胞内细菌流产布鲁氏菌中吸取的教训。","authors":"Ana María Rodríguez, Julia Rodríguez, Alex D Guano, Guillermo H Giambartolomei","doi":"10.1159/000548181","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Devoid of a lymphatic system, the central nervous system (CNS) relies primarily on innate immunity for protection. While these immune responses help to fight pathogens, they can also cause irreversible damage because of the CNS's limited regenerative capacity. Therefore, it is crucial to understand which CNS cells contribute to pathogen clearance but in doing so potentially damage surrounding tissue.</p><p><strong>Summary: </strong>Neurobrucellosis, caused by intracellular bacteria from the genus Brucella, is an inflammatory disease. Recent studies have shown that astrocytes and microglia are the source of this neuro-inflammation. In response to Brucella infection they create a microenvironment in the CNS which leads to the destabilization of the glial structure, the damage of the blood-brain barrier (BBB) and neuronal demise. Using Brucella as an example, this review of CNS glial cells responses to an intracellular bacterium shows how inflammation generates damage on tissue instead of infection resolution.</p><p><strong>Key messages: </strong>Since the network of pathophysiological interactions described here are not necessarily limited to brucellosis, it is reasonable to assume that these mechanisms could be relevant in other neurological disorders in which inflammation plays a key role.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1-24"},"PeriodicalIF":2.4000,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Damage on CNS cells elicited by innate immune activation: lessons to be learnt from the intracellular bacterium Brucella abortus.\",\"authors\":\"Ana María Rodríguez, Julia Rodríguez, Alex D Guano, Guillermo H Giambartolomei\",\"doi\":\"10.1159/000548181\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Devoid of a lymphatic system, the central nervous system (CNS) relies primarily on innate immunity for protection. While these immune responses help to fight pathogens, they can also cause irreversible damage because of the CNS's limited regenerative capacity. Therefore, it is crucial to understand which CNS cells contribute to pathogen clearance but in doing so potentially damage surrounding tissue.</p><p><strong>Summary: </strong>Neurobrucellosis, caused by intracellular bacteria from the genus Brucella, is an inflammatory disease. Recent studies have shown that astrocytes and microglia are the source of this neuro-inflammation. In response to Brucella infection they create a microenvironment in the CNS which leads to the destabilization of the glial structure, the damage of the blood-brain barrier (BBB) and neuronal demise. Using Brucella as an example, this review of CNS glial cells responses to an intracellular bacterium shows how inflammation generates damage on tissue instead of infection resolution.</p><p><strong>Key messages: </strong>Since the network of pathophysiological interactions described here are not necessarily limited to brucellosis, it is reasonable to assume that these mechanisms could be relevant in other neurological disorders in which inflammation plays a key role.</p>\",\"PeriodicalId\":19133,\"journal\":{\"name\":\"Neuroimmunomodulation\",\"volume\":\" \",\"pages\":\"1-24\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-08-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuroimmunomodulation\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1159/000548181\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroimmunomodulation","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000548181","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0

摘要

背景:缺乏淋巴系统,中枢神经系统(CNS)主要依靠先天免疫保护。虽然这些免疫反应有助于对抗病原体,但由于中枢神经系统的再生能力有限,它们也会造成不可逆转的损害。因此,了解哪些中枢神经系统细胞有助于病原体清除,但这样做可能会损害周围组织是至关重要的。摘要:神经布鲁氏菌病是一种由布鲁氏菌属细胞内细菌引起的炎症性疾病。最近的研究表明,星形胶质细胞和小胶质细胞是这种神经炎症的来源。为了应对布鲁氏菌感染,它们在中枢神经系统中创造了一个微环境,导致神经胶质结构的不稳定,血脑屏障(BBB)的破坏和神经元的死亡。以布鲁氏菌为例,本文回顾了中枢神经系统胶质细胞对细胞内细菌的反应,展示了炎症如何对组织产生损伤而不是感染消退。关键信息:由于这里描述的病理生理相互作用网络并不一定局限于布鲁氏菌病,因此有理由假设这些机制可能与炎症起关键作用的其他神经系统疾病有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Damage on CNS cells elicited by innate immune activation: lessons to be learnt from the intracellular bacterium Brucella abortus.

Background: Devoid of a lymphatic system, the central nervous system (CNS) relies primarily on innate immunity for protection. While these immune responses help to fight pathogens, they can also cause irreversible damage because of the CNS's limited regenerative capacity. Therefore, it is crucial to understand which CNS cells contribute to pathogen clearance but in doing so potentially damage surrounding tissue.

Summary: Neurobrucellosis, caused by intracellular bacteria from the genus Brucella, is an inflammatory disease. Recent studies have shown that astrocytes and microglia are the source of this neuro-inflammation. In response to Brucella infection they create a microenvironment in the CNS which leads to the destabilization of the glial structure, the damage of the blood-brain barrier (BBB) and neuronal demise. Using Brucella as an example, this review of CNS glial cells responses to an intracellular bacterium shows how inflammation generates damage on tissue instead of infection resolution.

Key messages: Since the network of pathophysiological interactions described here are not necessarily limited to brucellosis, it is reasonable to assume that these mechanisms could be relevant in other neurological disorders in which inflammation plays a key role.

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
Neuroimmunomodulation
Neuroimmunomodulation 医学-免疫学
CiteScore
3.60
自引率
4.20%
发文量
35
审稿时长
>12 weeks
期刊介绍: The rapidly expanding area of research known as neuroimmunomodulation explores the way in which the nervous system interacts with the immune system via neural, hormonal, and paracrine actions. Encompassing both basic and clinical research, ''Neuroimmunomodulation'' reports on all aspects of these interactions. Basic investigations consider all neural and humoral networks from molecular genetics through cell regulation to integrative systems of the body. The journal also aims to clarify the basic mechanisms involved in the pathogenesis of the CNS pathology in AIDS patients and in various neurodegenerative diseases. Although primarily devoted to research articles, timely reviews are published on a regular basis.
×
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