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Cited by 497Sepsis Diagnosis and TreatmentRedox biology and oxidative stressNitric Oxide and Endothelin Effects

Oxidative stress and gene expression in sepsis

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Macdonald, J., Galley, H.F., Webster, N.R.·2003·British Journal of Anaesthesia
DOI 10.1093/bja/aeg034
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Abstract

Dysregulation of the immuno-inflammatory response, as seen in sepsis, may culminate in host cell and organ damage. Lipopolysaccharide from Gram-negative bacterial cell walls induces gene activation and subsequent inflammatory mediator expression. Gene activation is regulated by a number of transcription factors at the nuclear level, of which nuclear factor kappaB appears to have a central role. The redox (reduction-oxidation) cellular balance is important for normal cellular function, including transcription factor regulation. In sepsis, a state of severe oxidative stress is encountered, with host endogenous antioxidant defences overcome. This has implications for cellular function and the regulation of gene expression. This review gives an overview of the mechanisms by which transcription factor activation and inflammatory mediator overexpression occur in sepsis, together with the events surrounding the state of oxidative stress encountered and the effects on the host's antioxidant defences. The effect of oxidative stress on transcription factor regulation is considered, together with the role of antioxidant repletion in transcription factor activation and in sepsis in general. Other interventions that may modulate transcription factor activation are also highlighted.

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Crossref · 10.1093/bja/aeg034

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107 of 107 references verified0 citation errors · 0 not checkable

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  • In the NF-κB system, NF-κB is normally held inactive in the cytoplasm by binding to an inhibitor IκB; pro-inflammatory cytokines such as TNF-α, LPS and IL-1 act by binding to receptors at the cell surface and initiating signalling pathways that lead to activation of IKK; IKK phosphorylates IκB causing its release and degradation, allowing NF-κB to translocate to the nucleus where it can activate a

    “In the NF-κB system (e.g. [2020-2024]) (Fig 8), NF-κB is normally held inactive in the cytoplasm by binding to an inhibitor IκB (often IκBα). Pro-inflammatory cytokines such as TNF-α, LPS [2025-2030] and IL-1 [2031] act by binding to receptors at the cell surface and initiating signalling pathways that lead to the activation of a particular kinase, IκB kinase or IKK. This kinase phosphorylates the”

    From Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases (2009) · cites this paper as [2028]

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Authors
Macdonald, J., Galley, H. F., & Webster, N. R.
Affiliations
University of Aberdeen (GB)
Corresponding author
Galley, H.F.
ORCID
Galley, H.F.
Venue
British Journal of Anaesthesia
Publisher
Elsevier BV
Published
2003-02
Volume
90
Issue
2
Pages
221-232
ISSN
0007-0912 (ISSN-L)
DOI
10.1093/bja/aeg034
OpenAlex
W2098866603
Cited by
497
References
107
Citations by year
2026: 9 · 2025: 9 · 2024: 10 · 2023: 9 · 2022: 16 · 2021: 20 · 2020: 32 · 2019: 20 · 2018: 28 · 2017: 20 · 2016: 34 · 2015: 19 · 2014: 23 · 2013: 33 · 2012: 21
FWCI
3.50
Type
journal article
Language
en
Open access
Licence
Locations
  • British Journal of Anaesthesia (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
sepsis, oxidative stress, gene expression, lipopolysaccharide, Gram-negative bacteria, NF-κB, transcription factors, antioxidant defense, inflammatory mediators, redox homeostasis, antioxidant supplementation, host immune response
MeSH terms
Animals, Antioxidants, Ascorbic Acid, Binding Sites, Dimethyl Sulfoxide, Gene Expression Regulation, Glutathione, Humans, Lipopolysaccharides, Oxidation-Reduction, Oxygen, Promoter Regions, Genetic, Transcription, Genetic, Vitamin E, Transcriptional Activation, Gene Expression, NF-kappa B, Reactive Oxygen Species, Oxidative Stress, Sepsis

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