Abstract
Heparin is used for inhibition of blood clotting but also has effects on inflammation. Heparin has been reported to inhibit allergen or exercise-induced bronchospasm in asthma, and to reduce rectal bleeding and inflammation in patients with ulcerative colitis [1–3]. Animal studies with heparin in numerous models of inflammation and cellmediated immunity have shown similar anti-inflammatory activity [4–6]. Despite evidence that heparin interferes with leukocyte migration, and particularly the adhesion of leukocytes to endothelial cells and endothelial transmigration, the mechanism for its anti-inflammatory effects in humans is unknown [7–11]. We report that treatment with unfractionated heparin increases the number of circulating lymphocytes in humans. This effect appears to be specific for CD4+ T cell subsets. We suggest that the effect of heparin on T cell migration may be one mechanism by which heparin exerts an antiinflammatory effect.
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