Ana María Rodríguez, Julia Rodríguez, Alex D Guano, Guillermo H Giambartolomei
{"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}
引用次数: 0
Abstract
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.
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.