[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.
Nogimura
Manami
M
Pulmonary Division, Second Department of Internal Medicine, Saitama Medical School.
Nagata
Makoto
M
Sutani
Akihisa
A
Saito
Keiko
K
Sakamoto
Yoshio
Y
D002448:Cell Adhesion / Q000187:drug effects*; D002867:Chromones / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004804:Eosinophils / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D066298:In Vitro Techniques; D020024:Leukotriene Antagonists / Q000494:pharmacology*; D008565:Membrane Proteins; D018077:Receptors, Leukotriene
D002867:Chromones; D020024:Leukotriene Antagonists; D008565:Membrane Proteins; D018077:Receptors, Leukotriene; C412375:cysteinyl leukotriene receptor 2; C083169:leukotriene D4 receptor; C047681:pranlukast