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Interleukin-1beta up-regulates tumor necrosis factor receptors in the mouse airways.

Cardell, Lars-Olaf LU ; Uddman, Rolf LU ; Zhang, Yaping LU and Adner, Mikael LU (2008) In Pulmonary Pharmacology & Therapeutics May 2. p.675-681
Abstract
Cytokines like interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha), released during the inflammatory process, play important roles in the development of airway hyperresponsiveness. The effects of these cytokines are mediated by cell surface receptors, specific for each cytokine. The expression of cytokine receptors is a dynamic process, where receptors can be up- or down-regulated in response to changes in the environment. One such environmental factor is the presence of cytokines per se. The present study was designed to evaluate the effects of IL-1beta on the expression of its corresponding receptor IL-1 RI, as well as on the closely related TNFalpha receptors TNF RI and TNF RII in airways using a mouse organ culture... (More)
Cytokines like interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha), released during the inflammatory process, play important roles in the development of airway hyperresponsiveness. The effects of these cytokines are mediated by cell surface receptors, specific for each cytokine. The expression of cytokine receptors is a dynamic process, where receptors can be up- or down-regulated in response to changes in the environment. One such environmental factor is the presence of cytokines per se. The present study was designed to evaluate the effects of IL-1beta on the expression of its corresponding receptor IL-1 RI, as well as on the closely related TNFalpha receptors TNF RI and TNF RII in airways using a mouse organ culture assay and intranasal inoculation model. Immunohistochemical staining was used to quantify expressional differences between fresh and cultured tracheal segments. In the fresh, uncultured, segments, IL-1 RI and TNF RI were seen in the epithelial layer and TNF RI in the smooth muscle layer. After 4 days of culture, the expression of TNF RI decreased in the epithelial layer, whereas the corresponding expression of IL-1 RI and TNF RI in the smooth muscle remained unchanged. When culture was performed in the presence of IL-1beta, the expression of IL-1 RI and TNF RI in the epithelial cells and TNF RI in the smooth muscle cells increased. TNF RII was not detected in either fresh or cultured trachea, but after treatment with IL-1beta an expression was found in both the epithelial layer and in the smooth muscle cells. The IL-1beta-induced increased expression, on TNF RI and TNF RII in the smooth muscle ex vivo and in the lung parenchyma after intranasal challenge in vivo, was verified at the mRNA level using real-time RT PCR. To summarize, presence of IL-1beta increases the expression of IL-1 R1 and TNF RI and induces expression of TNF RII in the airway wall. It is not inconceivable that these alterations of the IL-1 and TNF receptors may have important functional implications for the development of hyperresponsiveness in inflammatory airway diseases like asthma. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pulmonary Pharmacology & Therapeutics
volume
May 2
pages
675 - 681
publisher
Elsevier
external identifiers
  • WOS:000262943900014
  • PMID:18515164
  • Scopus:47249109331
ISSN
1522-9629
DOI
10.1016/j.pupt.2008.04.002
language
English
LU publication?
yes
id
066bb054-f318-4101-8d21-e538fdc786ba (old id 1169369)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18515164?dopt=Abstract
date added to LUP
2008-07-02 11:05:20
date last changed
2017-01-01 07:54:31
@article{066bb054-f318-4101-8d21-e538fdc786ba,
  abstract     = {Cytokines like interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha), released during the inflammatory process, play important roles in the development of airway hyperresponsiveness. The effects of these cytokines are mediated by cell surface receptors, specific for each cytokine. The expression of cytokine receptors is a dynamic process, where receptors can be up- or down-regulated in response to changes in the environment. One such environmental factor is the presence of cytokines per se. The present study was designed to evaluate the effects of IL-1beta on the expression of its corresponding receptor IL-1 RI, as well as on the closely related TNFalpha receptors TNF RI and TNF RII in airways using a mouse organ culture assay and intranasal inoculation model. Immunohistochemical staining was used to quantify expressional differences between fresh and cultured tracheal segments. In the fresh, uncultured, segments, IL-1 RI and TNF RI were seen in the epithelial layer and TNF RI in the smooth muscle layer. After 4 days of culture, the expression of TNF RI decreased in the epithelial layer, whereas the corresponding expression of IL-1 RI and TNF RI in the smooth muscle remained unchanged. When culture was performed in the presence of IL-1beta, the expression of IL-1 RI and TNF RI in the epithelial cells and TNF RI in the smooth muscle cells increased. TNF RII was not detected in either fresh or cultured trachea, but after treatment with IL-1beta an expression was found in both the epithelial layer and in the smooth muscle cells. The IL-1beta-induced increased expression, on TNF RI and TNF RII in the smooth muscle ex vivo and in the lung parenchyma after intranasal challenge in vivo, was verified at the mRNA level using real-time RT PCR. To summarize, presence of IL-1beta increases the expression of IL-1 R1 and TNF RI and induces expression of TNF RII in the airway wall. It is not inconceivable that these alterations of the IL-1 and TNF receptors may have important functional implications for the development of hyperresponsiveness in inflammatory airway diseases like asthma.},
  author       = {Cardell, Lars-Olaf and Uddman, Rolf and Zhang, Yaping and Adner, Mikael},
  issn         = {1522-9629},
  language     = {eng},
  pages        = {675--681},
  publisher    = {Elsevier},
  series       = {Pulmonary Pharmacology & Therapeutics},
  title        = {Interleukin-1beta up-regulates tumor necrosis factor receptors in the mouse airways.},
  url          = {http://dx.doi.org/10.1016/j.pupt.2008.04.002},
  volume       = {May 2},
  year         = {2008},
}