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Staphylococcus aureus enterotoxin B regulates prostaglandin E-2 synthesis, growth, and migration in nasal tissue fibroblasts

Claudina Perez Novo, Anouk Waeytens UGent, Cindy Claeys, Paul Van Cauwenberge and Claus Bachert UGent (2008) JOURNAL OF INFECTIOUS DISEASES. 197(7). p.1036-1043
abstract
Background. Superantigens and eicosanoids are important amplifiers and regulators of inflammation in airway diseases. We therefore studied the possible influence of Staphylococcus aureus enterotoxin B ( SEB) on the cyclooxygenase ( COX) pathway and basic functions of airway structural cells. Methods. Fibroblasts were isolated from nasal inferior turbinate tissue and cultured in the presence of different concentrations of SEB. Preincubation with interferon ( IFN)-gamma was performed to induce expression of major histocompatibility complex ( MHC) class II receptors. Prostaglandin E2 ( PGE(2)) production was assayed by enzyme-linked immunosorbent assay, and levels of COX-2 and prostanoid E receptors 1-4 ( EP1-4) were assayed by real-time polymerase chain reaction. Migration and growth tests were performed, and SEB was localized within the cells by confocal microscopy. Results. Stimulation with IFN-gamma and SEB significantly down-regulated PGE2, COX-2, and EP2 expression but not EP1, EP3, or EP4 expression. The enterotoxin blocked cell growth but increased the fibroblast migration rate. SEB was localized within the cell in the presence and absence of MHC-II, suggesting that mechanisms other than conventional binding may allow the enterotoxin to enter the cell. Conclusions. These findings may have major implications for our understanding of the role played by bacterial superantigens in regulating the inflammatory and remodeling mechanisms of upper airway diseases and hence may help elucidate the pathophysiology of these diseases.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
RHINOSINUSITIS, EXPRESSION, POLYPOSIS, INFLAMMATION, CELL-LINE, HUMAN LUNG FIBROBLASTS, INTERFERON-GAMMA, ICAM-1, SITE, CD40
journal title
JOURNAL OF INFECTIOUS DISEASES
J. Infect. Dis.
volume
197
issue
7
pages
1036-1043 pages
Web of Science type
Article
Web of Science id
000254249500016
JCR category
INFECTIOUS DISEASES
JCR impact factor
5.682 (2008)
JCR rank
5/51 (2008)
JCR quartile
1 (2008)
ISSN
0022-1899
DOI
1854/10730
language
English
UGent publication?
yes
classification
A1
id
408713
handle
http://hdl.handle.net/1854/LU-408713
date created
2008-05-15 10:22:00
date last changed
2016-12-19 15:43:05
@article{408713,
  abstract     = {Background. Superantigens and eicosanoids are important amplifiers and regulators of inflammation in airway diseases. We therefore studied the possible influence of Staphylococcus aureus enterotoxin B ( SEB) on the cyclooxygenase ( COX) pathway and basic functions of airway structural cells. 
Methods. Fibroblasts were isolated from nasal inferior turbinate tissue and cultured in the presence of different concentrations of SEB. Preincubation with interferon ( IFN)-gamma was performed to induce expression of major histocompatibility complex ( MHC) class II receptors. Prostaglandin E2 ( PGE(2)) production was assayed by enzyme-linked immunosorbent assay, and levels of COX-2 and prostanoid E receptors 1-4 ( EP1-4) were assayed by real-time polymerase chain reaction. Migration and growth tests were performed, and SEB was localized within the cells by confocal microscopy. 

Results. Stimulation with IFN-gamma and SEB significantly down-regulated PGE2, COX-2, and EP2 expression but not EP1, EP3, or EP4 expression. The enterotoxin blocked cell growth but increased the fibroblast migration rate. SEB was localized within the cell in the presence and absence of MHC-II, suggesting that mechanisms other than conventional binding may allow the enterotoxin to enter the cell. 

Conclusions. These findings may have major implications for our understanding of the role played by bacterial superantigens in regulating the inflammatory and remodeling mechanisms of upper airway diseases and hence may help elucidate the pathophysiology of these diseases.},
  author       = {Perez Novo, Claudina and Waeytens, Anouk and Claeys, Cindy and Van Cauwenberge, Paul and Bachert, Claus},
  issn         = {0022-1899},
  journal      = {JOURNAL OF INFECTIOUS DISEASES},
  keyword      = {RHINOSINUSITIS,EXPRESSION,POLYPOSIS,INFLAMMATION,CELL-LINE,HUMAN LUNG FIBROBLASTS,INTERFERON-GAMMA,ICAM-1,SITE,CD40},
  language     = {eng},
  number       = {7},
  pages        = {1036--1043},
  title        = {Staphylococcus aureus enterotoxin B regulates prostaglandin E-2 synthesis, growth, and migration in nasal tissue fibroblasts},
  url          = {http://dx.doi.org/1854/10730},
  volume       = {197},
  year         = {2008},
}

Chicago
Perez Novo, Claudina, Anouk Waeytens, Cindy Claeys, Paul Van Cauwenberge, and Claus Bachert. 2008. “Staphylococcus Aureus Enterotoxin B Regulates Prostaglandin E-2 Synthesis, Growth, and Migration in Nasal Tissue Fibroblasts.” Journal of Infectious Diseases 197 (7): 1036–1043.
APA
Perez Novo, C., Waeytens, A., Claeys, C., Van Cauwenberge, P., & Bachert, C. (2008). Staphylococcus aureus enterotoxin B regulates prostaglandin E-2 synthesis, growth, and migration in nasal tissue fibroblasts. JOURNAL OF INFECTIOUS DISEASES, 197(7), 1036–1043.
Vancouver
1.
Perez Novo C, Waeytens A, Claeys C, Van Cauwenberge P, Bachert C. Staphylococcus aureus enterotoxin B regulates prostaglandin E-2 synthesis, growth, and migration in nasal tissue fibroblasts. JOURNAL OF INFECTIOUS DISEASES. 2008;197(7):1036–43.
MLA
Perez Novo, Claudina, Anouk Waeytens, Cindy Claeys, et al. “Staphylococcus Aureus Enterotoxin B Regulates Prostaglandin E-2 Synthesis, Growth, and Migration in Nasal Tissue Fibroblasts.” JOURNAL OF INFECTIOUS DISEASES 197.7 (2008): 1036–1043. Print.