EXPRESSION OF FUNCTIONAL VCAM-1 BY CULTURED NASAL POLYP-DERIVED MICROVASCULAR ENDOTHELIUM

Induction of endothelial vascular cell adhesion molecule-1 (VCAM-1) by interleukin (IL)-4 is believed to exert a major impact oil the extrav asation of leukocyte subsets in allergic disease, This notion has rece ntly been challenged because cultured microvascular endothelial cells (ECs) derived from various organs are unable to express VCAM-1 after e xposure to IL-4, In this study, we have established a method for isola tion and culture of nasal polyp-derived microvascular ECs and report t heir cytokine-regulated VCAM-1 expression, With a combination of cell enzyme-linked immunosorbent assay, flow cytometry, and reverse transcr iption polymerase chain reaction, such expression was shown to be indu ced in a dose- and time-dependent manner not only by IL-1 beta and tum or necrosis factor-alpha but also by IL-4 and IL-13, Therefore, the re sponse of nasal microvascular ECs did not harmonize with that of count erparts from several other tissues, IL-4 or IL-13 combined with submax imal concentrations of IL-1 beta or tumor necrosis factor-alpha increa sed VCAM-1 expression in a synergistic manner. VCAM-1 was functional a s shown by antibody-mediated inhibition of leukocyte adhesion. Taken t ogether, our results supported the notion that selective VCAM-1 induct ion by 11-4 and IL-13 plays an important role for the preferential rec ruitment of eosinophils and T lymphocytes seen in human airways affect ed by allergy.