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中枢神经系统炎症对神经元损伤的影响:一段无声的历史。

Effect of Systemic Inflammation in the CNS: A Silent History of Neuronal Damage.

机构信息

Red MEDICI, Carrera Médico Cirujano, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de Mexico, Tlalnepantla 54090, Mexico.

Laboratory of Immunobiology and Genetics, Instituto Nacional de Enfermedades Respiratorias Ismael Cos'ıo Villegas, Mexico City 14080, Mexico.

出版信息

Int J Mol Sci. 2023 Jul 25;24(15):11902. doi: 10.3390/ijms241511902.

DOI:10.3390/ijms241511902
PMID:37569277
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10419139/
Abstract

Central nervous system (CNS) infections including meningitis and encephalitis, resulting from the blood-borne spread of specific microorganisms, provoke nervous tissue damage due to the inflammatory process. Moreover, different pathologies such as sepsis can generate systemic inflammation. Bacterial lipopolysaccharide (LPS) induces the release of inflammatory mediators and damage molecules, which are then released into the bloodstream and can interact with structures such as the CNS, thus modifying the blood-brain barrier's (BBB´s) and blood-cerebrospinal fluid barrier´s (BCSFB´s) function and inducing aseptic neuroinflammation. During neuroinflammation, the participation of glial cells (astrocytes, microglia, and oligodendrocytes) plays an important role. They release cytokines, chemokines, reactive oxygen species, nitrogen species, peptides, and even excitatory amino acids that lead to neuronal damage. The neurons undergo morphological and functional changes that could initiate functional alterations to neurodegenerative processes. The present work aims to explain these processes and the pathophysiological interactions involved in CNS damage in the absence of microbes or inflammatory cells.

摘要

中枢神经系统(CNS)感染包括脑膜炎和脑炎,是由特定微生物经血源性传播引起的,由于炎症过程会导致神经组织损伤。此外,败血症等不同的病理情况也会引发全身炎症。细菌脂多糖(LPS)诱导炎症介质和损伤分子的释放,这些物质随后被释放到血液中,并与 CNS 等结构相互作用,从而改变血脑屏障(BBB)和血脑脊液屏障(BCSFB)的功能,并诱导无菌性神经炎症。在神经炎症过程中,神经胶质细胞(星形胶质细胞、小胶质细胞和少突胶质细胞)的参与起着重要作用。它们释放细胞因子、趋化因子、活性氧、活性氮、肽,甚至兴奋性氨基酸,导致神经元损伤。神经元发生形态和功能改变,可能引发神经退行性过程中的功能改变。本工作旨在解释这些过程以及在没有微生物或炎症细胞的情况下 CNS 损伤涉及的病理生理相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/d4757e69ed25/ijms-24-11902-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/b08267556f12/ijms-24-11902-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/59cce58a7a28/ijms-24-11902-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/e17fef0285b6/ijms-24-11902-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/d4757e69ed25/ijms-24-11902-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/b08267556f12/ijms-24-11902-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/59cce58a7a28/ijms-24-11902-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/e17fef0285b6/ijms-24-11902-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75b6/10419139/d4757e69ed25/ijms-24-11902-g004.jpg

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