Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism

Mov Disord. 2005 Jul;20(7):843-5. doi: 10.1002/mds.20418.

Abstract

The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody-mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement-inactivated serum from SC patients was associated with a significant increase in Ca2+ levels evoked by KCl stimulus (mean +/- SEM, 341.0 +/- 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 +/- 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca2+ levels determined by SC patients sera correlated directly with the enzyme-linked immunosorbent assay optical density values for anti-basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Animals
  • Antibodies / pharmacology
  • Basal Ganglia / immunology
  • Calcium / metabolism*
  • Child
  • Chorea / blood*
  • Chorea / immunology
  • Complement System Proteins / pharmacology*
  • Enzyme-Linked Immunosorbent Assay / methods
  • Female
  • Humans
  • Intracellular Fluid / metabolism*
  • Microscopy, Confocal / methods
  • PC12 Cells / drug effects*
  • Potassium Chloride / pharmacology
  • Rats
  • Serum / metabolism*

Substances

  • Antibodies
  • Potassium Chloride
  • Complement System Proteins
  • Calcium