Expression of adhesion molecules on cord-blood-derived, cultured human mast cells and effect of dexamethasone on intercellular adhesion molecule-1 expression on the mast cells treated by phorbol myristate acetate.

BACKGROUND

Increase in mast-cell number at sites of allergic inflammation has been observed, and glucocorticoids applied to the sites have been shown to result in a significant reduction in mast cells. However, the expression of adhesion molecules on cultured human mast cells and their regulation by glucocorticoids is poorly understood.

METHODS

Cultured human mast cells were raised from human umbilical cord-blood cells, and the expression of adhesion molecules on the mast cells was analyzed by flow cytometry. The cells were also incubated with 10 ng/ml phorbol myristate acetate (PMA) for the indicated time, and the effect of dexamethasone on adhesion molecule expression on PMA-treated, cultured human mast cells was examined.

RESULTS

Cord-blood-derived, cultured human mast cells constitutively expressed intercellular adhesion molecule-1 (ICAM-1), very late antigen-4 (VLA-4), and macrophage-1 antigen (Mac-1). Weak expression of lymphocyte function-associated antigen-1 (LFA-1) was observed on the cells, whereas they failed to express vascular cell adhesion molecule-1 (VCAM-1). Kinetic studies showed that after a transient downregulation reaching a minimum at 8 h, the expression of ICAM-1 was markedly upregulated on PMA-treated mast cells after a 24-h incubation. In contrast, the expression of VLA-4 and Mac-1 was decreased after the incubation with PMA for 24 h. The PMA-induced upregulation of ICAM-1 was inhibited by dexamethasone in a concentration-dependent manner.

CONCLUSION

Our results indicate that cord-blood-derived, cultured human mast cells constitutively express integrins and ICAM-1, but not VCAM-1, and demonstrate for the first time that dexamethasone inhibits the upregulation of ICAM-1 on PMA-treated, cultured human mast cells.