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Related Experiment Videos

Adhesion molecule expression in venous leg ulcers

J C Veraart1, M E Verhaegh, H A Neumann

  • 1Department of Dematology, University Hospital Maastricht, The Netherlands.

VASA. Zeitschrift Fur Gefasskrankheiten
|January 1, 1993
PubMed
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Chronic venous insufficiency ulcers show altered expression of adhesion molecules, impacting inflammatory responses and wound healing. This suggests insufficient monocyte and lymphocyte migration crucial for healing venous leg ulcers.

Area of Science:

  • Dermatology
  • Vascular Biology
  • Wound Healing Research

Background:

  • Chronic venous insufficiency (CVI) culminates in ulceration, a complex condition with incompletely understood pathomechanisms.
  • Adhesion molecules are critical mediators of inflammatory processes and are implicated in wound healing.
  • Previous theories do not fully explain the diverse skin alterations observed in CVI.

Purpose of the Study:

  • To investigate the expression of key adhesion molecules: intercellular adhesion molecule-1 (ICAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), and vascular cellular adhesion molecule-1 (VCAM-1) in venous leg ulcers.
  • To correlate adhesion molecule expression with inflammatory responses and cellular infiltration in the ulcer microenvironment.

Main Methods:

  • Skin biopsies were obtained from the perilesional skin of 8 patients with venous leg ulcers.

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  • Immunohistochemical analysis was performed to assess the expression patterns of ICAM-1, ELAM-1, and VCAM-1 on endothelial cells and infiltrating leukocytes.
  • Expression levels were compared between ulcerated areas and surrounding perilesional skin.

    • Main Results:

    • ICAM-1 exhibited weak to moderate expression on capillaries beneath the ulcer and moderate expression in the papillary dermis around the ulcer.
    • A strong expression of ELAM-1 was localized to capillaries within the inflammatory infiltrate directly under the ulcer, with moderate expression observed peripherally.
    • VCAM-1 expression was notably absent in all investigated venous leg ulcer specimens.

    Conclusions:

    • The findings indicate a dysregulated inflammatory response in venous leg ulcers, characterized by altered adhesion molecule expression.
    • Insufficient adhesion and migration of monocytes and lymphocytes to the wound area may impair the initiation of healing in the perilesional skin.
    • These results highlight a potential molecular basis for impaired wound healing in CVI.