[Study on the effect of cysteinyl leukotriene antagonist, pranlukast hydrate, on adhesive interaction between eosinophils and pulmonary endothelial cells].
It has been reported that cysteinyl leukotriene (CysLT) antagonists reduce the accumulation of eosinophils in the asthmatic airway. However, the exact mechanism of this action remains to be established. In the present study, we examined whether a CysLT antagonist modifies the adhesive interaction between blood eosinophils and endothelial cells. Pranlukast hydrate, a CysLT antagonist, blocked the chemotactic response and adhesion of eosinophils induced by LTD4. On the other hand, pranlukast did not modify the eosinophil spontaneous adhesion to the resting or IL-4 plus TNF-alpha-stimulated pulmonary endothelial cells. Similarly, pranlukast did not modulate IL-5- or FMLP-activated eosinophil adhesion to the resting endothelial cells. Finally, pranlukast did not modify the expression of adhesion molecules on endothelial cells stimulated with endothelial activating cytokines. These results suggest that the inhibitory action of CysLT antagonist on eosinophil accumulation in the asthmatic airways involves mechanisms other than the adhesive interaction between eosinophils and endothelial cells.
T10 T11 T12 T13 T14 T15 T1 T2 T3 T4 T5 T6 T7 T8 T9
CHEMICAL CHEMICAL CHEMICAL GENE-Y GENE-Y GENE-Y CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL
CysLT cysteinyl leukotriene pranlukast hydrate IL-4 TNF-alpha IL-5 CysLT cysteinyl leukotriene Pranlukast hydrate CysLT LTD4 pranlukast CysLT pranlukast pranlukast