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The choroid plexus response to peripheral inflammatory stimulus.

F Marques1, J C Sousa, M Correia-Neves

  • 1Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal.

Neuroscience
|October 31, 2006
PubMed
Summary
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The choroid plexus (CP) responds to systemic inflammation by increasing prostaglandin D2 synthase (LPTGDS) levels. This suggests the CP acts as a key mediator of immune signals from the periphery to the brain.

Area of Science:

  • Neuroimmunology
  • Cerebrospinal Fluid Dynamics
  • Brain Inflammation

Background:

  • The choroid plexus (CP) forms a critical barrier between blood and cerebrospinal fluid (CSF).
  • Its role in mediating brain responses to peripheral inflammation is understudied.
  • CP capillaries are fenestrated, allowing molecular and cellular passage.

Purpose of the Study:

  • To investigate how systemic inflammation affects gene expression of constitutively expressed proteins in the mouse choroid plexus.
  • To determine the role of the CP in the brain's inflammatory response.

Main Methods:

  • Mice were subjected to a systemic inflammatory stimulus (lipopolysaccharide administration).
  • Quantitative analysis of messenger RNA (mRNA) levels for CP proteins.

Related Experiment Videos

  • Measurement of LPTGDS levels in cerebrospinal fluid (CSF).

    • Main Results:

    • Systemic inflammation rapidly induced pro-inflammatory cytokine mRNA (interleukin-1 beta, tumor necrosis factor-alpha) in the CP.
    • mRNA for transthyretin and transferrin remained unchanged.
    • Prostaglandin D2 synthase (LPTGDS) mRNA and CSF levels were significantly upregulated post-inflammation.

    Conclusions:

    • The choroid plexus actively responds to peripheral inflammatory signals.
    • Upregulation of LPTGDS suggests its involvement in mediating inflammatory communication between the periphery and the brain.
    • The CP should be recognized as a significant mediator in neuroinflammatory processes.