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Pb Induces MCP-1 in the Choroid Plexus.

Huiying Gu1, Yundan Xu1,2, Nicole Du3

  • 1Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

Biology
|February 25, 2022
PubMed
Summary

Lead exposure triggers monocyte chemoattractant protein-1 (MCP-1) expression and macrophage infiltration in the brain's choroid plexus. This occurs via p38 and NF-κB pathways, contributing to neuroinflammation in Alzheimer's disease.

Keywords:
Alzheimer’s diseaseMCP-1NF-κBZ310choroid plexusleadmacrophage infiltrationp38 MAP kinase

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Area of Science:

  • Neuroscience
  • Toxicology
  • Immunology

Background:

  • Lead (Pb) exposure is linked to dementia and Alzheimer's disease (AD).
  • Innate immune activation is a key factor in AD, but mechanisms are unclear.
  • The choroid plexus (CP) is crucial for cerebrospinal fluid (CSF) production and brain-blood barrier function.

Purpose of the Study:

  • To investigate the role of the choroid plexus (CP) in lead (Pb) exposure.
  • To evaluate the expression of monocyte chemoattractant protein-1 (MCP-1) in the CP during Pb exposure.
  • To elucidate the molecular pathways involved in Pb-induced neuroinflammation.

Main Methods:

  • Assessed MCP-1 expression and macrophage infiltration in the CP following Pb exposure.
  • Utilized cultured Z310 rat CP cells to study Pb effects.
  • Investigated the involvement of NF-κB and p38 MAP kinase pathways using specific inhibitors (SB 203580 and BAY 11-7082).

Main Results:

  • Pb exposure significantly increased MCP-1 expression and macrophage infiltration in the CP.
  • Pb exposure dose-dependently stimulated MCP-1 expression in CP cells.
  • Pb activated both NF-κB and p38 MAP kinase pathways, which were crucial for MCP-1 induction.

Conclusions:

  • Pb exposure stimulates MCP-1 expression in the CP through p38 and NF-κB p65 pathways.
  • This process is associated with increased macrophage infiltration into the CP.
  • Findings suggest a novel mechanism linking Pb exposure to neuroinflammation relevant to AD pathogenesis.