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Optineurin deficiency in mice is associated with increased sensitivity to Salmonella but does not affect proinflammatory NF-κB signaling

Karolina Slowicka UGent, Lars Vereecke UGent, Conor Mc Guire UGent, Mozes Sze UGent, Jonathan Maelfait UGent, Annasaheb Kolpe UGent, Xavier Saelens UGent, Rudi Beyaert UGent and Geert van Loo UGent (2016) EUROPEAN JOURNAL OF IMMUNOLOGY. 46(4). p.971-980
abstract
Optineurin (OPTN) is an evolutionary conserved and ubiquitously expressed ubiquitin-binding protein that has been implicated in glaucoma, Paget bone disease, amyotrophic lateral sclerosis, and other neurodegenerative diseases. From in vitro studies, OPTN was shown to suppress TNF-induced NF-kappa B signaling and virus-induced IRF signaling, and was identified as an autophagy receptor required for the clearance of cytosolic Salmonella upon infection. To assess the in vivo functions of OPTN in inflammation and infection, we generated OPTN-deficient mice. OPTN knockout mice are born with normal Mendelian distribution and develop normally without any signs of spontaneous organ abnormality or inflammation. However, no differences in NF-kappa B activation could be observed in OPTN knockoutmice or fibroblasts derived from thesemice upon TNF or LPS treatment. Primary bone marrow-derived macrophages from OPTN-deficient mice had slightly impaired IRF signaling and reduced IFN type I production in response to LPS or poly(I, C). Finally, OPTN-deficient mice were more susceptible to infection with Salmonella, confirming in vivo the importance of OPTN in bacterial clearance.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
Inflammation, Autophagy, Innate immunity, Interferon, NF-kappa B, Optineurin, AMYOTROPHIC-LATERAL-SCLEROSIS, AUTOPHAGY RECEPTOR OPTINEURIN, OPEN-ANGLE GLAUCOMA, SELECTIVE AUTOPHAGY, ACTIVATION, BINDING, GENE, PHOSPHORYLATION, DISRUPTION, EXPRESSION
journal title
EUROPEAN JOURNAL OF IMMUNOLOGY
Eur. J. Immunol.
volume
46
issue
4
pages
971 - 980
Web of Science type
Article
Web of Science id
000374552700019
JCR category
IMMUNOLOGY
JCR impact factor
4.227 (2016)
JCR rank
40/150 (2016)
JCR quartile
2 (2016)
ISSN
0014-2980
DOI
10.1002/eji.201545863
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
7176875
handle
http://hdl.handle.net/1854/LU-7176875
date created
2016-04-06 14:06:01
date last changed
2016-12-19 15:42:08
@article{7176875,
  abstract     = {Optineurin (OPTN) is an evolutionary conserved and ubiquitously expressed ubiquitin-binding protein that has been implicated in glaucoma, Paget bone disease, amyotrophic lateral sclerosis, and other neurodegenerative diseases. From in vitro studies, OPTN was shown to suppress TNF-induced NF-kappa B signaling and virus-induced IRF signaling, and was identified as an autophagy receptor required for the clearance of cytosolic Salmonella upon infection. To assess the in vivo functions of OPTN in inflammation and infection, we generated OPTN-deficient mice. OPTN knockout mice are born with normal Mendelian distribution and develop normally without any signs of spontaneous organ abnormality or inflammation. However, no differences in NF-kappa B activation could be observed in OPTN knockoutmice or fibroblasts derived from thesemice upon TNF or LPS treatment. Primary bone marrow-derived macrophages from OPTN-deficient mice had slightly impaired IRF signaling and reduced IFN type I production in response to LPS or poly(I, C). Finally, OPTN-deficient mice were more susceptible to infection with Salmonella, confirming in vivo the importance of OPTN in bacterial clearance.},
  author       = {Slowicka, Karolina and Vereecke, Lars and Mc Guire, Conor and Sze, Mozes and Maelfait, Jonathan and Kolpe, Annasaheb and Saelens, Xavier and Beyaert, Rudi and van Loo, Geert},
  issn         = {0014-2980},
  journal      = {EUROPEAN JOURNAL OF IMMUNOLOGY},
  keyword      = {Inflammation,Autophagy,Innate immunity,Interferon,NF-kappa B,Optineurin,AMYOTROPHIC-LATERAL-SCLEROSIS,AUTOPHAGY RECEPTOR OPTINEURIN,OPEN-ANGLE GLAUCOMA,SELECTIVE AUTOPHAGY,ACTIVATION,BINDING,GENE,PHOSPHORYLATION,DISRUPTION,EXPRESSION},
  language     = {eng},
  number       = {4},
  pages        = {971--980},
  title        = {Optineurin deficiency in mice is associated with increased sensitivity to Salmonella but does not affect proinflammatory NF-\ensuremath{\kappa}B signaling},
  url          = {http://dx.doi.org/10.1002/eji.201545863},
  volume       = {46},
  year         = {2016},
}

Chicago
Slowicka, Karolina, Lars Vereecke, Conor Mc Guire, Mozes Sze, Jonathan Maelfait, Annasaheb Kolpe, Xavier Saelens, Rudi Beyaert, and Geert van Loo. 2016. “Optineurin Deficiency in Mice Is Associated with Increased Sensitivity to Salmonella but Does Not Affect Proinflammatory NF-κB Signaling.” European Journal of Immunology 46 (4): 971–980.
APA
Slowicka, K., Vereecke, L., Mc Guire, C., Sze, M., Maelfait, J., Kolpe, A., Saelens, X., et al. (2016). Optineurin deficiency in mice is associated with increased sensitivity to Salmonella but does not affect proinflammatory NF-κB signaling. EUROPEAN JOURNAL OF IMMUNOLOGY, 46(4), 971–980.
Vancouver
1.
Slowicka K, Vereecke L, Mc Guire C, Sze M, Maelfait J, Kolpe A, et al. Optineurin deficiency in mice is associated with increased sensitivity to Salmonella but does not affect proinflammatory NF-κB signaling. EUROPEAN JOURNAL OF IMMUNOLOGY. 2016;46(4):971–80.
MLA
Slowicka, Karolina, Lars Vereecke, Conor Mc Guire, et al. “Optineurin Deficiency in Mice Is Associated with Increased Sensitivity to Salmonella but Does Not Affect Proinflammatory NF-κB Signaling.” EUROPEAN JOURNAL OF IMMUNOLOGY 46.4 (2016): 971–980. Print.