BRADYKININ-B1 AND BRADYKININ-B2 RECEPTOR AGONISTS SYNERGISTICALLY POTENTIATE INTERLEUKIN-1-INDUCED PROSTAGLANDIN BIOSYNTHESIS IN HUMAN GINGIVAL FIBROBLASTS

被引：68

作者：

LERNER, UH ^{[1
]}

MODEER, T ^{[1
]}

机构：

[1] KAROLINSKA INST, FAC ODONTOL, DEPT PEDODONT, S-10401 STOCKHOLM 60, SWEDEN

来源：

INFLAMMATION | 1991年 / 15卷 / 06期

关键词：

D O I：

10.1007/BF00923340

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The interactions between bradykinin (BK) and interleukin-1 (IL-1) on prostaglandin formation in human gingival fibroblasts have been studied. IL-1-alpha and IL-1-beta stimulated prostaglandin E2 (PGE2) formation in the gingival fibroblasts with IL-1-beta being the most potent agonist. The effects of both IL-1-alpha and IL-1-beta on PGE2 biosynthesis was synergistically potentiated by BK, in a dose-related manner. The synergistic interaction between IL-1-beta and BK on PGE2 Production was seen both with B1 (des-Arg9-BK) and B2 (BK, Lys-BK) BK receptor agonists. No synergistic interaction between BK and IL-1-beta was seen on arachidonic acid release. These data suggest that BK and IL-1 act in concert to enhance prostanoid formation in inflammatory lesions and that the level of interaction is distal to phospholipase activity.

引用

页码：427 / 436

页数：10

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