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Author Spotlight: Insight Into Advances in Prion Diseases Research
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Adipose-derived mesenchymal stromal cells decrease prion-induced glial inflammation in vitro.

Arielle J D Hay1,2, Tanner J Murphy1,2,3, Katriana A Popichak1,2,4

  • 1Prion Research Center, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, 80523, USA.

Scientific Reports
|December 29, 2022
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Summary
This summary is machine-generated.

Adipose-derived mesenchymal stromal cells (AdMSCs) reduce prion-induced brain inflammation by producing anti-inflammatory molecules. These cells reprogram glial cells to a protective state, offering a potential therapeutic strategy for early-stage prion diseases.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Prion diseases involve prion protein (PrPSc) misfolding, leading to neurodegeneration.
  • Early disease stages feature neuroinflammation, with glial cell activation.
  • Current therapeutics do not effectively target this early inflammatory phase.

Purpose of the Study:

  • To investigate the therapeutic potential of adipose-derived mesenchymal stromal cells (AdMSCs) in mitigating prion-induced neuroinflammation.
  • To determine if AdMSCs can modulate glial cell responses in a prion disease model.

Main Methods:

  • AdMSCs were tested for migration towards prion-infected brain homogenate.
  • AdMSCs' production of anti-inflammatory molecules (TGFβ, TSG-6) was analyzed.
  • In vitro co-culture models using primary mixed glia and BV2 microglial cells exposed to prion were employed.
  • Changes in inflammatory cytokine mRNA and glial activation markers were quantified.

Main Results:

  • AdMSCs migrated towards prion-infected brain homogenate and secreted TGFβ and TSG-6.
  • Co-culturing with AdMSCs significantly reduced inflammatory cytokine mRNA levels.
  • AdMSCs decreased markers of reactive astrocytes and activated microglia.
  • The protective effects were observed independently of PrPSc replication.

Conclusions:

  • AdMSCs demonstrate potential as a therapeutic agent for prion diseases by reducing early glial inflammation.
  • AdMSCs can reprogram glial cells towards a protective phenotype, counteracting detrimental inflammatory responses.
  • This approach offers a novel strategy targeting the initial inflammatory cascade in prion diseases.