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Related Experiment Videos

Cytokines in sickle cell disease.

Anil Pathare1, Salam Al Kindi, Shahina Daar

  • 1Department of Hematology, College of Medicine, Sultan Qaboos University, Muscat, Sultanate of Oman. avp16@hotmail.com

Hematology (Amsterdam, Netherlands)
|October 8, 2003
PubMed
Summary

Sickle cell disease involves activated blood cells and endothelium, leading to cell adhesion and vasoocclusion. This complex cellular activation underlies the painful vasoocclusive crises characteristic of sickle cell disease.

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Area of Science:

  • Hematology
  • Vascular Biology
  • Immunology

Background:

  • Sickle red blood cells express adhesion molecules, promoting binding to endothelial cells.
  • Activated sickle monocytes, polymorphonuclear leukocytes (PMNs), and platelets contribute to endothelial activation and inflammation.
  • Endothelial cell activation results in loss of vascular integrity and a prothrombotic state.

Purpose of the Study:

  • To elucidate the molecular mechanisms of cellular activation in sickle cell disease.
  • To understand the role of cell-cell interactions in the pathogenesis of vasoocclusion.

Main Methods:

  • Analysis of adhesion molecule expression on sickle red cells, monocytes, PMNs, and platelets.
  • Assessment of cytokine release and endothelial cell activation markers.

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  • Investigation of cell-aggregate formation and endothelial-extracellular matrix interactions.

    • Main Results:

    • Sickle cells, monocytes, PMNs, and platelets exhibit increased expression of adhesion molecules and activation markers.
    • Proinflammatory cytokines (TNF-alpha, IL-1beta) are elevated.
    • Activated endothelial cells upregulate adhesion molecules, HLA molecules, and expose extracellular matrix proteins, facilitating vasoocclusion.

    Conclusions:

    • Multiple cellular interactions and activation pathways contribute to endothelial dysfunction in sickle cell disease.
    • These processes culminate in vasoocclusion and tissue ischemia, forming the basis of vasoocclusive crisis.