Regulation of kinin receptors in airway epithelial cells by inflammatory cytokines and dexamethasone
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- 作者：Newton ; Robert ; Eddleston ; Jane ; Haddad ; El-Bdaoui ; Hawisa ; Samia ; Mak ; Judith ; Lim ; Sam ; Fox ; Alison J. ; et. al.
- 关键词：Bradykinin ; Des-Arg10-kallidin ; Bradykinin B1 receptor ; Bradykinin B2 receptor ; Cyclooxygenase ; Epithelial cell ; Dexamethasone
- 刊名：European Journal of Pharmacology
- 出版年：2002
- 出版时间：April 26, 2002
- 年：2002
- 卷：441
- 期：3
- 页码：193-202
- 全文大小：480 K
文摘
The two kinin receptors, B1 and B2, are upregulated in inflammation and may play a role in diseases such as asthma. In pulmonary A549 cells, TNF-α or interleukin-1β dramatically increased bradykinin B1 and B2 receptor mRNA expression and this response was prevented by dexamethasone. In primary human bronchial epithelial cells, bradykinin B1 receptor mRNA expression showed a similar trend, whereas bradykinin B2 receptor showed almost constitutive expression. Radioligand-binding studies revealed significant increases in bradykinin B2 receptor protein expression following both interleukin-1β and TNF-α treatment of A549 cells; however, no evidence was found for bradykinin B1 receptor. Functionally, the bradykinin B2 receptor ligand, bradykinin, but not the B1 ligand, des-Arg10-kallidin, produced a marked increase in prostaglandin E2 release when administered following interleukin-1β treatment. Arachidonic acid release in response to bradykinin was markedly enhanced by prior incubation with interleukin-1β and this was prevented by the prior addition of dexamethasone.