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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pharmacology

Background:

  • Cholesterol crystals (CC) drive atherosclerosis by activating inflammatory pathways like the complement system and inflammasome.
  • Cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (BCD) is known to solubilize lipophilic substances and has shown anti-inflammatory effects.
  • The impact of BCD on CC-induced complement activation was previously unknown.

Purpose of the Study:

  • To investigate the effects of BCD on complement activation induced by cholesterol crystals (CC).
  • To determine if BCD can mitigate the inflammatory responses triggered by CC in human plasma and blood.

Main Methods:

  • BCD was incubated with CC in human plasma and whole blood to assess its effects on complement deposition and activation.
  • Measurements included Ig and complement factor deposition, terminal complement complex formation, and complement receptor expression on monocytes.
  • Reactive oxygen species (ROS) formation and pro-inflammatory cytokine release (IL-1α, MIP-1α, TNF, IL-6, IL-8) were analyzed.
  • Gene expression of complement-related factors in human carotid plaques was examined ex vivo.

Main Results:

  • BCD bound to CC, reducing the deposition of Igs, pattern recognition molecules, and complement factors.
  • BCD significantly decreased terminal complement complex formation and lowered complement receptor expression on monocytes.
  • BCD attenuated CC-induced ROS production and pro-inflammatory cytokine release in whole blood.
  • BCD modulated complement-related gene expression in human carotid plaques but did not affect complement activation on other structures.

Conclusions:

  • BCD effectively inhibits cholesterol crystal-induced inflammation by attenuating complement activation.
  • BCD demonstrates potential as a therapeutic agent for treating atherosclerosis by targeting CC-mediated inflammatory pathways.