Regulation of kinin B(2) receptors by bradykinin in human lung cells.
Författare
Summary, in English
Abstract Bradykinin is a potent mediator of inflammation that has been shown to participate in allergic airway inflammation. The biologic effects of bradykinin are mediated by binding and activating its cognate receptor, the B(2) receptor (B(2)R). In the lung fibroblast cell line IMR-90, binding of bradykinin to the B(2)R triggers down-regulation of the receptor surface expression, suggesting that bradykinin-induced inflammation is transient and self-limited. Notably, subjects with chronic airway inflammation continue to respond to BK following a first challenge. B(2)Rs are expressed on many different lung cell types, including airway epithelial cells. We therefore compared IMR-90 cells with the human lung epithelial cell line BEAS2B and found that B2R expression in the two cell types is differently regulated by BK. While BK induces a down-regulation of B(2)R in IMR-90 cells, the same treatment leads to an up-regulation of the receptor in BEAS2B cells. These results provide a possible explanation for the potency of bradykinin in inducing ongoing airway inflammation.
Avdelning/ar
Publiceringsår
2008
Språk
Engelska
Sidor
1435-1440
Publikation/Tidskrift/Serie
Biological Chemistry
Volym
389
Länkar
Dokumenttyp
Artikel i tidskrift
Förlag
De Gruyter
Ämne
- Infectious Medicine
Status
Published
ISBN/ISSN/Övrigt
- ISSN: 1437-4315