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Complement activation in sickle cell disease: a liposome model.

M A Tomasko1, D S Chudwin

  • 1Department of Immunology/Microbiology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612.

The Journal of Laboratory and Clinical Medicine
|August 1, 1988
PubMed
Summary
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Abnormal red blood cell membranes in sickle cell disease (SCD) may cause chronic alternative complement pathway (ACP) activation. This study used liposomes to show altered phospholipids on sickle cells activate the ACP.

Area of Science:

  • Biochemistry
  • Hematology
  • Immunology

Background:

  • Patients with sickle cell disease (SCD) exhibit poorly understood abnormalities in their alternative complement pathway (ACP).
  • Previous research indicated chronic ACP activation in SCD patients.

Purpose of the Study:

  • To investigate the mechanism behind chronic ACP activation in SCD.
  • To determine if abnormal phospholipid organization in sickle cells contributes to ACP activation.

Main Methods:

  • Serum concentrations of complement control proteins (factors I and H) were measured in SCD patients and controls.
  • A liposome model was employed to assess ACP activation by sickle cell membrane phospholipids.
  • Liposomes mimicked the phospholipid composition of sickle cell outer and inner leaflets.

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Main Results:

  • No significant difference in factors I and H concentrations was found between SCD patients and controls.
  • Liposomes mimicking sickle cell outer leaflet phospholipids (enriched in phosphatidylserine and phosphatidylethanolamine) significantly increased ACP activation.
  • Liposomes mimicking the erythrocyte inner membrane leaflet also showed enhanced ACP activation compared to normal outer leaflet liposomes.

Conclusions:

  • Phospholipid composition of cell membranes influences their ability to promote ACP activation.
  • Altered phospholipid organization in sickle cells likely contributes to the chronic ACP activation observed in sickle cell disease.