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Astroglia in Sepsis Associated Encephalopathy

Authors
  • Shulyatnikova, Tatyana1
  • Verkhratsky, Alexei2, 3, 4
  • 1 Zaporizhzhia State Medical University, Zaporizhzhya, 69035, Ukraine , Zaporizhzhya (Ukraine)
  • 2 The University of Manchester, Manchester, M13 9PT, UK , Manchester (United Kingdom)
  • 3 University of Copenhagen, Copenhagen, 2200, Denmark , Copenhagen (Denmark)
  • 4 IKERBASQUE, Basque Foundation for Science, Bilbao, 48011, Spain , Bilbao (Spain)
Type
Published Article
Journal
Neurochemical Research
Publisher
Springer-Verlag
Publication Date
Feb 18, 2019
Volume
45
Issue
1
Pages
83–99
Identifiers
DOI: 10.1007/s11064-019-02743-2
Source
Springer Nature
Keywords
License
Yellow

Abstract

Cellular pathophysiology of sepsis associated encephalopathy (SAE) remains poorly characterised. Brain pathology in SAE, which is manifested by impaired perception, consciousness and cognition, results from multifactorial events, including high levels of systemic cytokines, microbial components and endotoxins, which all damage the brain barriers, instigate neuroinflammation and cause homeostatic failure. Astrocytes, being the principal homeostatic cells of the central nervous system contribute to the brain defence against infection. Forming multifunctional anatomical barriers, astroglial cells maintain brain-systemic interfaces and restrict the damage to the nervous tissue. Astrocytes detect, produce and integrate inflammatory signals between immune cells and cells of brain parenchyma, thus regulating brain immune response. In SAE astrocytes are present in both reactive and astrogliopathic states; balance between these states define evolution of pathology and neurological outcomes. In humans pathophysiology of SAE is complicated by frequent presence of comorbidities, as well as age-related remodelling of the brain tissue with senescence of astroglia; these confounding factors further impact upon SAE progression and neurological deficits.

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