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Cited by 77Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersThermal Regulation in Medicine

Correction: A Systematic Analysis of the Peripheral and CNS Effects of Systemic LPS, IL-1Β, TNF-α and IL-6 Challenges in C57BL/6 Mice

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Skelly, Donal T., Hennessy, Edel, Dansereau, Marc-Andre, Cunningham, Colm·2013·PLoS ONE
DOI 10.1371/annotation/90c76048-2edd-4315-8404-4d9d8cbd411ePMC PMC3861548
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Abstract

It is increasingly clear that systemic inflammation has both adaptive and deleterious effects on the brain.However, detailed comparisons of brain effects of systemic challenges with different pro-inflammatory cytokines are lacking.In the present study, we challenged female C57BL/6 mice intraperitoneally with LPS (100 µg/kg), IL-1β (15 or 50 µg/kg), TNF-α (50 or 250 µg/kg) or IL-6 (50 or 125 µg/kg).We investigated effects on core body temperature, open field activity and plasma levels of inflammatory markers at 2 hours post injection.We also examined levels of hepatic, hypothalamic and hippocampal inflammatory cytokine transcripts.Hypothermia and locomotor hypoactivity were induced by LPS>IL-1β>TNF-α>>IL-6.Systemic LPS, IL-1β and TNF-α challenges induced robust and broadly similar systemic and central inflammation compared to IL-6, which showed limited effects, but did induce a hepatic acute phase response.Important exceptions included IFNβ, which could only be induced by LPS.Systemic IL-1β could not induce significant blood TNF-α, but induced CNS TNF-α mRNA, while systemic TNF-α could induce IL-1β in blood and brain.Differences between IL-1β and TNF-α-induced hippocampal profiles, specifically for IL-6 and CXCL1 prompted a temporal analysis of systemic and central responses at 1, 2, 4, 8 and 24 hours, which revealed that IL-1β and TNF-α both induced the chemokines CXCL1 and CCL2 but only IL-1β induced the pentraxin PTX3.Expression of COX-2, CXCL1 and CCL2, with nuclear localisation of the p65 subunit of NFκB, in the cerebrovasculature was demonstrated by immunohistochemistry. Furthermore, we used cFOS immunohistochemistry to show that LPS, IL-1β and to a lesser degree, TNF-α activated the central nucleus of the amygdala.Given the increasing attention in the clinical literautre on correlating specific systemic inflammatory mediators with neurological or neuropsychiatric conditions and complications, these data will provide a useful resource on the likely CNS inflammatory profiles resulting from systemic elevation of particular cytokines.

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  • MoMg that derive from HSC expressing the DNMT3A R822H variant cause a motor impairment reminiscent of the hypokinetic motor phenotype seen in parkinsonism.

    “Specifically, using a BM transfer model, we show that MoMg that derive from HSC that express the DNMT3A R822H variant cause a motor impairment reminiscent of the hypokinetic motor phenotype seen in parkinsonism 72 .”

    From Clonal hematopoiesis-associated motoric deficits caused by monocyte-derived microglia accumulating in aging mice (2025) · cites this paper as [72]

    The Sickness behaviour section (page unavailable) reports reduced locomotor activity after systemic inflammatory challenges in mice, not a parkinsonian motor phenotype. The passages found for DNMT3A R822H, bone-marrow transfer, and hypokinetic parkinsonism do not address the comparison for which this citation appears to be offered; the variant-specific result is framed as the citing authors’ own finding. (LLM, conf=0.75)

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Authors
Skelly, D. T., Hennessy, E., Dansereau, M.-A., & Cunningham, C.
Affiliations
Virginia Commonwealth University (US)
Corresponding author
Cunningham, Colm
ORCID
Venue
PLoS ONE
Publisher
Public Library of Science (PLoS)
Published
2013-12-09
Volume
8
Issue
12
ISSN
1932-6203 (ISSN-L)
DOI
10.1371/annotation/90c76048-2edd-4315-8404-4d9d8cbd411e
PMC
PMC3861548
OpenAlex
W2629368404
Cited by
77
References
20
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Type
journal article
Language
en
Open access
Licence
Locations
  • PLoS ONE (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Wellcome Trust
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Thermal Regulation in Medicine
Keywords
systemic inflammation, lipopolysaccharide, IL-1β, TNF-α, interleukin-6, inflammatory cytokines, neuroinflammation, core body temperature, hypothermia, acute phase response, CXCL1, MCP-1, cyclooxygenase-2, NF-κB, amygdala, C57BL/6 mice

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Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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