Affiliations: University Hospital for Dermatology, Fleischmannstr. 42‐44, D‐17487 Greifswald, Germany | Department of Dermatology, University Hospital Tübingen, Liebermeisterstr. 25, D‐72076 Tübingen, Germany | Department of Physiology I, University of Tübingen, Gmelinstr. 5, D‐72076 Tübingen, Germany | Section of Immunohaematology and Transplantation Immunology, Department of Medicine, University Hospital Tübingen, Otfried‐Müller‐Str. 10, D‐72076 Tübingen, Germany | Department of Bioengineering and Institute for Biomedical Engineering, University of California at San Diego, La Jolla, CA 92093‐0412, USA
Note: [] Corresponding author: Prof. Dr. med. Michael Jünger, University Hospital for Dermatology, Fleischmannstr. 42‐44, D‐17487 Greifswald, Germany. Tel.: +49 3834 86 6770; Fax: +49 3834 86 6772; E‐mail: juenger@uni‐greifswald.de.
Abstract: In this study we analysed blood samples taken from the dorsalis pedis vein and a brachial vein of 11 healthy test persons and 8 patients with venous leg ulcer under experimental venous hypertension in order to examine changes in the expression of leukocyte adhesion molecules (LFA‐1 (CD11a), Mac‐1 (CD11b), p150,95 (CD11c), CD18, VLA‐4 (CD49d) and L‐selectin (CD62L)) which are involved in the adhesion steps of leukocytes to endothelial cells for transmigration into tissues. Under orthostatic stress, lymphocytes in controls collected at the foot level showed a significant reduction in the expression of L‐selectin (p=0.002), compared to those of patients. This finding suggests that venous stasis negatively influences the expression of L‐selectin on leukocytes only in healthy volunteers. Patients with chronic venous insufficiency seem to suffer from a specific defect in the regulation of L‐selectin shedding under orthostatic stress.
Keywords: Varicose‐ulcer pathophysiology, varicose‐ulcer immunology, venous leg ulcer, leukocyte‐adhesion‐molecules
