ArticleImmunology2011
An in vitro experimental model of neuroinflammation: the induction of interleukin-6 in murine astrocytes infected with Theiler's murine encephalomyelitis virus, and its inhibition by oestrogenic receptor modulators.
Article in Immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 14 citations in OpenAlex.
- Regulating cell fate of human amnion epithelial cells using natural compounds: an example of enhanced neural and pigment differentiation by 3,4,5-tri-O-caffeoylquinic acid.Cell communication and signaling : CCS · 2021Article
- Neurotoxic potential of reactive astrocytes in canine distemper demyelinating leukoencephalitis.Scientific reports · 2019Article
- Using gene expression signatures to identify novel treatment strategies in gulf war illness.BMC medical genomics · 2015Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This paper describes an experimental model of neuroinflammation based on the production of interleukin-6 (IL-6) by neural glial cells infected with Theiler's murine encephalomyelitis virus (TMEV). Production of IL-6 mRNA in mock-infected and TMEV-infected SJL/J murine astrocytes was examined using the Affymetrix murine genome U74v2 DNA microarray. The IL-6 mRNA from infected cells showed an eightfold increase in hybridization to a sequence encoding IL-6 located on chromosome number 5. Quantitative real-time reverse transcription PCR (qPCR) was used to study the regulation of IL-6 expression. The presence of IL-6 in the supernatants of TMEV-infected astrocyte cultures was quantified by ELISA and found to be weaker than in cultures of infected macrophages. The IL-6 was induced by whole TMEV virions, but not by Ad.βGal adenovirus, purified TMEV capsid proteins, or UV-inactivated virus. Two recombinant inflammatory cytokines, IL-1α and tumour necrosis factor-α were also found to be potent inducers of IL-6. The secreted IL-6 was biologically active because it fully supported B9 hybridoma proliferation in a [(3) H]thymidine incorporation bioassay. The cerebrospinal fluid of infected mice contained IL-6 during the acute encephalitis phase, peaking at days 2-4 post-infection. Finally, this in vitro neuroinflammation model was fully inhibited, as demonstrated by ELISA and qPCR, by five selective oestrogen receptor modulators.
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