Induction of endothelial vascular cell adhesion molecule-1 (VCAM-1) by interleukin (IL)-4 is believed to exert a major impact on the extravasation of leukocyte subsets in allergic disease. This notion has recently been challenged because cultured microvascular endothelial cells (ECs) derived from various organs are unable to express VCAM-1 after exposure to IL-4. In this study, we have established a method for isolation and culture of nasal polyp-derived microvascular ECs and report their cytokine-regulated VCAM-1 expression. With a combination of cell enzyme-linked immunosorbent assay, flow cytometry, and reverse transcription polymerase chain reaction, such expression was shown to be induced in a dose- and time-dependent manner not only by IL-1 beta and tumor necrosis factor-alpha but also by IL-4 and IL-13. Therefore, the response of nasal microvascular ECs did not harmonize with that of counterparts from several other tissues. IL-4 or IL-13 combined with submaximal concentrations of IL-1 beta or tumor necrosis factor-alpha increased VCAM-1 expression in a synergistic manner. VCAM-1 was functional as shown by antibody-mediated inhibition of leukocyte adhesion. Taken together, our results supported the notion that selective VCAM-1 induction by IL-4 and IL-13 plays an important role for the preferential recruitment of eosinophils and T lymphocytes seen in human airways affected by allergy.