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Complement-dependent phagocytosis of liposomes

N M Wassef1, C R Alving

  • 1Department of Membrane Biochemistry, Walter Reed Army Institute of Research, Washington, DC 20307-5100.

Chemistry and Physics of Lipids
|September 1, 1993
PubMed
Summary

Certain lipids and factors like negative charge suppress complement-dependent phagocytosis of liposomes. This suppression may explain the extended circulation time of stealth liposomes in vivo.

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Area of Science:

  • Lipid nanoparticle research
  • Immunology
  • Drug delivery systems

Background:

  • Complement-opsonized liposomes are typically phagocytosed by macrophages.
  • Certain lipids (e.g., phosphatidylinositol, GM1 ganglioside) are known to prolong liposome circulation time in vivo.

Purpose of the Study:

  • To investigate the in vitro model for complement-dependent phagocytosis of liposomes.
  • To identify factors that suppress liposome phagocytosis, potentially explaining prolonged circulation times.

Main Methods:

  • Utilized an in vitro model of complement-dependent phagocytosis using cultured macrophages.
  • Investigated the effect of specific lipids, liposomal charge, and prostaglandin content on phagocytosis.

Main Results:

  • Liposomes containing phosphatidylinositol, GM1 ganglioside, and sulfogalactosyl ceramide showed suppressed complement-dependent phagocytosis.
  • Increased liposomal negative charge and the presence of prostaglandin E2 or thromboxane B2 also suppressed phagocytosis.
  • These findings suggest mechanisms for reduced liposome clearance.

Conclusions:

  • Suppression of complement-dependent phagocytosis is linked to the prolonged circulation of 'stealth' liposomes.
  • Complement opsonization likely plays a role in the in vivo clearance of liposomes from circulation.

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