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Regulation of kinin B(2) receptors by bradykinin in human lung cells.

Bengtson, Sara LU ; Eddleston, Jane; Mörgelin, Matthias LU ; Zuraw, Bruce L and Herwald, Heiko LU (2008) In Biological Chemistry 389. p.1435-1440
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Biological Chemistry
volume
389
pages
1435 - 1440
publisher
De Gruyter
external identifiers
  • wos:000262137400011
  • pmid:18783336
  • scopus:56549105194
ISSN
1437-4315
DOI
10.1515/BC.2008.159
language
English
LU publication?
yes
id
195462df-9722-4a64-bc2d-73658f6e364f (old id 1243172)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18783336?dopt=Abstract
date added to LUP
2008-10-07 14:18:22
date last changed
2017-09-03 04:47:45
@article{195462df-9722-4a64-bc2d-73658f6e364f,
  abstract     = {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.},
  author       = {Bengtson, Sara and Eddleston, Jane and Mörgelin, Matthias and Zuraw, Bruce L and Herwald, Heiko},
  issn         = {1437-4315},
  language     = {eng},
  pages        = {1435--1440},
  publisher    = {De Gruyter},
  series       = {Biological Chemistry},
  title        = {Regulation of kinin B(2) receptors by bradykinin in human lung cells.},
  url          = {http://dx.doi.org/10.1515/BC.2008.159},
  volume       = {389},
  year         = {2008},
}